Substances and methods for improving intestinal health and homeostasis, nutrition and development in subjects

Abstract

Provided herein are materials and methods for improving intestinal health and homeostasis, nutrition and development in a subject. The substance is odd-carbon fatty acid. Specifically, the invention provides a method. The invention provides applications of odd-carbon fatty acid in preparation of drugs for increasing the protein expression abundance of closely linked related proteins of an object, reducing the content of corticotropin releasing hormone in intestinal tissues of the object, improving or enhancing the intestinal mechanical barrier of the object, maintaining the intestinal immune homeostasis of the object, and improving the immunity of the object. The composition is capable of promoting intestinal development of the object, maintaining energy steady state of intestinal cells of the object, improving intestinal energy metabolism, promoting development and metabolism of muscle tissues of the object, promoting development and metabolism of adipose tissues of the object, reducing allergic reaction of the body and intestinal tracts of the object, reducing insulin resistance of the object during pregnancy, controlling blood sugar of the object during pregnancy, and improving immunity of the object. The invention relates to application in preparations or medicines for preventing gestational diabetes mellitus, preventing or improving intrahepatic cholestasis of an object in a gestation period, preventing or treating diseases caused by helicobacter pylori bacteria and the like of the object.

Description

Technical Field

[0001] The present invention relates to materials and methods for improving intestinal health and homeostasis, subject nutrition and development. Background Art

[0002] Odd Carbon Fatty Acid (OCFA) is a type of fatty acid with an odd number of carbon atoms. A small amount of OCFA exists in natural lipids. They are a normal part of the animal body and can be metabolized normally in the body. The prior art generally believes that the accumulation of OCFA in the human body does not affect the normal growth and development of the human body.

[0003] Some studies have shown that odd-numbered fatty acids have different properties and physiological effects from even-numbered fatty acids: compared with even-numbered fatty acids, odd-numbered fatty acids have a looser crystal structure and weaker intermolecular forces; the metabolic pathways of odd-numbered fatty acids in the human body are different from those of even-numbered fatty acids, and the propionyl-CoA generated by β-oxidation has a glucogenic effect and is a dynamic endogenous indicator for human dietary assessment; pentadecanoic acid and heptadecanoic acid can be used to assess the risk of coronary heart disease and diabetes; pentadecanoic acid and nonadecanoic acid have a strong inhibitory effect on the growth of various cancer cells, etc. Summary of the invention

[0004] The present invention aims to develop new applications of odd-numbered carbon fatty acids or triglycerides containing odd-numbered carbon fatty acids.

[0005] Specifically, the present invention provides the use of odd-numbered carbon fatty acids in the preparation of preparations or medicines for any 1, any 2, any 3, any 4, any 5, any 6, any 7, any 8, any 9, any 10, any 11, any 12, any 13, any 14, any 15, any 16, any 17, any 18, any 19, any 20, any 21, any 22, any 23, any 24, any 25, any 26, any 27, any 28, any 29, any 30, any 31, any 32, any 33, any 34, any 35, any 36, any 37, any 38 or all 39 of the 39 items listed herein.

[0006] The present invention also provides grease for the above application.

[0007] The present invention is described in more detail below. BRIEF DESCRIPTION OF THE DRAWINGS

[0008] Figure 1 : Differences in the expression levels of multiple tight junction-related proteins in the duodenum, jejunum, and ileum of piglets fed with different lipid dietary supplements.

[0009] Figure 2 : Differences in ileal CRF levels in piglets fed with different oil dietary supplements.

[0010] Figure 3 : Differences in IgG, IgA, and IgM levels in the jejunum of piglets fed with different lipid dietary supplements.

[0011] Figure 4 : Differences in IgG, IgA, and IgM levels in the ileum of piglets fed with different lipid dietary supplements.

[0012] Figure 5 : Differences in protein expression levels of TLR4 and NF-κB in the duodenum, jejunum, and ileum of piglets fed with different oil dietary supplements.

[0013] Figure 6 : Differences in ileum levels of TNF-α, IL-1β, IL-6, and IL-10 in piglets fed with different oil dietary supplements.

[0014] Figure 7 : Differences in gene expression levels of MUC-2 in the ileum of piglets consuming different lipid dietary supplements.

[0015] Figure 8 : Differences in Ki67 protein expression levels in the duodenum, jejunum, and ileum of piglets fed with different lipid dietary supplements.

[0016] Fig. 9 : Differences in p-mTOR (phosphorylated mTOR) protein expression levels in the duodenum, jejunum, and ileum of piglets fed with different oil dietary supplements.

[0017] Fig.10 : Differences in p-p70S6K (phosphorylated p70S6K) protein expression levels in the duodenum, jejunum, and ileum of piglets fed with different oil dietary supplements.

[0018] Fig.11 : Differences in the levels of maltase in the duodenum and aminopeptidase N and sucrase in the ileum of piglets fed with different lipid dietary supplements.

[0019] Fig.12 : Differences in 5-HT levels in the duodenum, jejunum, and ileum and SP levels in the ileum of piglets fed with different oil dietary supplements.

[0020] Fig.13: Differences in protein expression levels of key mitophagy proteins ULK1, TFEB and Parkin in the duodenum and jejunum and ULK1 and TFEB in the ileum in piglets fed different oil dietary supplements.

[0021] Fig.14 : Differences in protein expression levels of PPARγ and SREBP-1 in the duodenum and jejunum of piglets fed with different oil dietary supplements.

[0022] Fig.15 : Differences in protein expression levels of MYHC 1, MYHC 2a, MYHC 2b, MYHC2x, mTOR, p-AMPK, and PGC1-α in dorsal muscle of piglets fed different oil dietary supplements.

[0023] Fig.16 : Differences in gene expression levels of SREBP-1C in dorsal muscle of piglets fed with different lipid dietary supplements.

[0024] Fig.17 : Differences in protein expression levels of p-mTOR (phosphorylated mTOR), Prdm16 and Irisin in back fat and p-mTOR and Prdm16 in perirenal fat of piglets fed different lipid dietary supplements.

[0025] Fig.18 : Differences in gene expression levels of SREBP-1C and APOB in back fat of piglets fed with different lipid dietary supplements.

[0026] Fig.19 : Differences in serum glutathione peroxidase (GSH-PX) levels in piglets fed with different oil dietary supplements.

[0027] Fig. 20 : Differences in the levels of IgE and HIS in serum, jejunum and ileum of piglets fed with different oil dietary supplements.

[0028] Fig.21 : The average daily weight gain, average daily feed intake and feed-to-weight ratio of piglets that consumed different oil dietary supplements during the trial period (the average daily feed intake and feed-to-weight ratio of the breast milk group G0 could not be accurately calculated).

[0029] Fig. 22 : Ratios of liver, cerebrum, cerebellum, and brainstem weight to body weight in piglets fed different lipid dietary supplements.

[0030] Fig.23 : Levels of serum cortisol and adrenocorticotropic hormone (ACTH) in piglets fed with different fat dietary supplements.

[0031] Fig.24 : Serum levels of HDL-C, LDL-C, ALT, AST, TG, and CHOL in piglets fed with different oil dietary supplements.

[0032] Fig.25 : Serum TP, ALB, BUN, and CREA levels in piglets fed with different lipid dietary supplements.

[0033] Fig.26 : Serum TNF-α levels in piglets fed with different lipid dietary supplements.

[0034] Fig. 27 : Serum IgG and IgM levels and spleen IgA levels in piglets fed with different oil dietary supplements.

[0035] Fig.28 : Serum D-LACT levels in piglets fed with different lipid dietary supplements.

[0036] Fig.29 :Fasting serum glucose (GLU), fasting serum insulin (INS) levels and fasting insulin resistance index in pregnant mice fed with different oils and diets.

[0037] Fig.30 : Serum bile acid levels in pregnant mice fed with different oils and diets.

[0038] Fig.31 : Levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and malondialdehyde (MDA) in the liver of pregnant mice consuming different oils and diets.

[0039] Fig.32 : Colon histological injury scores and colon HE staining images of pregnant mice consuming different oils and diets.

[0040] Fig.33 : Gene expression levels of colonic inflammatory factors IL-1β, IL-6, TNF-α, NLRP3, and GSDMD in pregnant mice consuming different oils and diets.

[0041] Fig.34 : The percentage levels of measured sequences of Helicobacter pylori and Deferribacter in the intestines of pregnant mice consuming different oils and diets.

[0042] Fig.35 : Feed-to-weight ratio of pregnant mice consuming different oils and diets during the experimental period.

[0043] Fig.36 : Serum TC, TG, HDL and LDL levels in pregnant mice consuming different oils and diets.

[0044] Fig.37 : Differences in protein expression levels of HIF-1α in the duodenum, jejunum, and ileum of piglets fed with different lipid dietary supplements.

[0045] Fig.38 : Scanning electron micrographs of the intestines of piglets fed with different lipid dietary supplements.

[0046] Fig.39 : HE staining of the intestine of piglets fed with different oil dietary supplements.

[0047] Fig.40 : Duodenal villus height, crypt depth and their ratio in piglets fed different lipid dietary supplements.

[0048] Fig.41 : Jejunal villus height, crypt depth and their ratio in piglets fed different lipid dietary supplements.

[0049] Fig.42 : Ileal villus height, crypt depth and their ratio in piglets fed different lipid dietary supplements.

[0050] In the above figures, * indicates P < 0.05, ** indicates P < 0.01, *** indicates P < 0.005, and ns indicates no significant difference. DETAILED DESCRIPTION

[0051] It should be understood that within the scope of the present invention, the above-mentioned various technical features of the present invention and the various technical features specifically described below (such as embodiments) can be combined with each other to form a preferred technical solution. Unless otherwise specified, the meanings of the terms used herein are the same as those generally understood by those skilled in the art. Unless otherwise specified, the various percentage contents (X%) and the ratios between the components used in this application are based on weight ratios.

[0052] The present application has studied the physiological and medical effects of odd-numbered carbon fatty acids and discovered new biological activities and functions of odd-numbered carbon fatty acids. Therefore, the present application aims to provide new applications of odd-numbered carbon fatty acids.

[0053] As used herein, "odd-numbered fatty acids" refer to fatty acids with an odd number of carbon atoms, including but not limited to C11:0 fatty acids (undecanoic acid), C13:0 fatty acids (tridecanoic acid), C15:0 fatty acids (pentadecanoic acid), C17:0 fatty acids (heptadecanoic acid), C19:0 fatty acids (nonadecanoic acid), C21:0 fatty acids (heneicosanoic acid), C23:0 fatty acids (tricosanoic acid) or any combination thereof. In some embodiments, the odd-numbered fatty acids described herein particularly include one or more of C11:0 fatty acids (undecanoic acid), C13:0 fatty acids (tridecanoic acid), C15:0 fatty acids (pentadecanoic acid) and C17:0 fatty acids (heptadecanoic acid), or consist of one or more of C11:0 fatty acids (undecanoic acid), C13:0 fatty acids (tridecanoic acid), C15:0 fatty acids (pentadecanoic acid) and C17:0 fatty acids (heptadecanoic acid).

[0054] In some embodiments, in the applications described herein, the content of C15:0 fatty acids is 80% or more, preferably 85%, 90% or more, or 95% or more, based on the total amount of odd-numbered fatty acids. In some embodiments, the content of C15:0 fatty acids is 99% or more, based on the total amount of odd-numbered fatty acids. In some embodiments, in the applications described herein, the odd-numbered fatty acids contain C17:0 in addition to C15:0; the content of C17:0 is ≤18% based on the total weight of odd-numbered fatty acids; in some embodiments, the content of C17:0 is ≤13%; in some embodiments, the content of C17:0 is ≤5%; in some embodiments, the content of C17:0 is ≤3%; in some embodiments, the content of C17:0 is ≤1%.

[0055] It should be understood that in the application of odd-numbered fatty acids described herein, odd-numbered fatty acids can be used in the form of odd-numbered fatty acids, or in the form of fatty acid chains contained in glycerides such as monoglycerides, diglycerides and / or triglycerides. In some embodiments, the triglycerides are oils and fats. As used herein, the percentage of a certain fatty acid content based on the total amount of odd-numbered fatty acids has the following conventional meanings: (1) when present in the form of fatty acids, the percentage of this fatty acid in the total amount of odd-numbered fatty acids; and (2) when present in the form of glycerides, the percentage of this fatty acid residue in the total amount of fatty acid residues attached to the glycerides. Unless otherwise indicated, the content herein is expressed by weight or weight percentage.

[0056] Therefore, in some embodiments, the present application provides the use of glycerides such as oils and fats containing odd-numbered carbon fatty acids in the fatty acid composition. Preferably, the glycerides, especially the fatty acid composition of oils and fats, have an odd-numbered carbon fatty acid content of ≥20%, such as 20-70% or 20-60%. Glycerides, especially the odd-numbered carbon fatty acids of oils and fats, can include any of the odd-numbered carbon fatty acids described above, preferably at least containing one or more of C11:0 fatty acids (undecanoic acid), C13:0 fatty acids (tridecanoic acid), C15:0 fatty acids (pentadecanoic acid) and C17:0 fatty acids (heptadecanoic acid), or composed of one or more of C11:0 fatty acids (undecanoic acid), C13:0 fatty acids (tridecanoic acid), C15:0 fatty acids (pentadecanoic acid) and C17:0 fatty acids (heptadecanoic acid). Preferably, the odd-numbered carbon fatty acids of glycerides, especially oils and fats, contain at least C15:0 fatty acids (pentadecanoic acid).

[0057] In the composition of odd-numbered fatty acids in glycerides, especially oils and fats, the content of C15:0 fatty acids is more than 80%, preferably more than 85%, more than 90% or more than 95%, based on the total amount of odd-numbered fatty acids. In some embodiments, the content of C15:0 fatty acids is more than 99% based on the total amount of odd-numbered fatty acids. In some embodiments, the odd-numbered fatty acids contain C17:0 in addition to C15:0; the content of C17:0 is ≤18% based on the total weight of odd-numbered fatty acids; in some embodiments, the content of C17:0 is ≤13%; in some embodiments, the content of C17:0 is ≤5%; in some embodiments, the content of C17:0 is ≤3%; in some embodiments, the content of C17:0 is ≤1%.

[0058] In some embodiments, in the fatty acid composition of the glyceride, especially the oil, the content of C11:0 fatty acid is not higher than 5%, preferably not higher than 1%, and more preferably not higher than 0.5%; the content of C13:0 fatty acid is 1-5%, preferably 2-4%; the content of C15:0 fatty acid is 15-70%, preferably 18-60%; the content of C17:0 fatty acid is 0.1-9%; the content of C19:0 fatty acid is not higher than 5%, preferably not higher than 1%, more preferably not higher than 0.5%; the content of C21:0 fatty acid is not higher than 5%, preferably not higher than 1%, more preferably not higher than 0.5%; the content of C23:0 fatty acid is not higher than 5%, preferably not higher than 1%, more preferably not higher than 0.5%.

[0059] In some embodiments, the fatty acid composition of the glyceride, especially the oil, also contains any one or more of C12:0, C14:0, C14:1, C16:0, C16:1, C18:0, C18:1, C18:2, C20:0, C18:3, C18:3T, C20:1, C20:2, C22:0, C20:3N6, C20:4N6, C20:5N3, C22:1, C20:3N3, C23:0, C22:2, C22:5, C22:6, C24:0 and C24:1. Preferably, in the fatty acid composition of the glyceride, especially the oil, the content of C16:0 may be 2-15%, such as 4-13%; the content of C18:0 may be ≤5%, such as 0-5% or 0-3%; the content of C18:1 may be 5-35%, such as 7-33%; the content of C18:2 may be ≤35%, such as 0-35%; the content of C22:5 may be ≤5%, such as 0-5% or 1-3.5%; the content of C22:6 may be 5-25%, such as 8-22%; the content of the remaining fatty acids is usually not more than 1% or less than 0.5%.

[0060] In some embodiments, in the fatty acid composition of the glyceride, especially the oil, the content of C13:0 is 1-5%, preferably 2-4%, the content of C15:0 is 40-60%, preferably 45-53%, the content of C16:0 is 1-7%, preferably 3-5.5%, the content of C17:0 is 4-9%, preferably 5-9%, the content of C18:1 is 5-10%, preferably 6-8%, the content of C22:5 is 1-5%, preferably 2-4%, the content of C22:6 is 15-25%, preferably 18-22%; the content of other fatty acids is usually less than 1% or less than 0.5%. In some embodiments, in the fatty acid composition of the glyceride, especially the oil, the content of C15:0 is 40-65%, preferably 50-60%, the content of C16:0 is 1-7%, preferably 3-5.5%, the content of C17:0 is 0.1-3%, preferably 0.1-1%, the content of C18:0 is 1-5%, preferably 1-3%, the content of C18:1 is 25-35%, preferably 28-34%, the content of C18:2 is 1-5%, preferably 2-4%; the content of other fatty acids is usually less than 1% or less than 0.5%.

[0061] In some embodiments, in the fatty acid composition of the glyceride, especially the oil, the content of C15:0 is 12-25%, preferably 16-22%, the content of C16:0 is 5-15%, preferably 10-15%, the content of C17:0 is 1-7%, preferably 2-5%, the content of C18:0 is 0.5-3%, preferably 1-2%, the content of C18:1 is 12-22%, preferably 15-20%, the content of C18:2 is 25-35%, preferably 30-35%, the content of C22:6 is 5-15%, preferably 7-12%; the content of other fatty acids is usually less than 1% or less than 0.5%.

[0062] It should be understood that the content of each fatty acid in the fatty acid composition described in this article is determined by referring to the third method "normalization method" in "GB5009.168-2016 National Food Safety Standard Determination of Fatty Acids in Food".

[0063] In some embodiments, the oil is derived from edible oil (e.g., one or more edible oils), transesterification products of edible oils, or any combination thereof. In some embodiments, triglycerides of odd-numbered fatty acids are prepared by transesterification with conventional edible oils.

[0064] In some embodiments, the edible oil is selected from vegetable oil, microbial oil, animal oil or any combination of the foregoing; preferably, the vegetable oil includes rice oil, sunflower oil (such as high oleic sunflower oil), rapeseed oil, palm oil, palm kernel oil, peanut oil, rapeseed oil, soybean oil, cottonseed oil, safflower seed oil, perilla seed oil, tea seed oil, olive oil, cocoa bean oil, Chinese tallow seed oil, almond oil, apricot kernel oil, tung seed oil, rubber seed oil, corn oil, wheat germ oil, sesame seed oil, castor seed oil, evening primrose seed oil, hazelnut oil, pumpkin seed oil, walnut oil, grape seed oil, borage seed oil, sea buckthorn seed oil, tomato seed oil, macadamia nut oil, coconut oil and cocoa butter, or its fractionation product, self-esterification product or esterification product of two or more oils; the animal oil is selected from lard, chicken fat, sheep fat, fish oil and beef tallow.

[0065] In some embodiments, the microorganism can be selected from: algae, such as strains of Thraustochytriales, more specifically, Thraustochytriales including Thraustochytrium and Schizochytrium sp. strains; oil-producing bacteria, such as Rhodococcus, such as Rhodococcus opacus; oil-producing yeast, such as Yarrowia, such as Yarrowia lipolytica; mutant strains derived from any of the above strains and mixed strains thereof. Preferably, the microorganism is Schizochytrium.

[0066] Transesterification includes chemical transesterification and enzymatic transesterification. For chemical transesterification, a chemical catalyst conventionally used for chemical transesterification can be selected for implementation. Exemplary chemical catalysts include, but are not limited to, acidic catalysts and alkaline catalysts. Preferably, the chemical catalyst is NaOH, KOH, NaOCH3, sodium ethoxide, an organic base, a solid base catalyst, sulfuric acid, a sulfonic acid or a solid acid catalyst; more preferably, the chemical catalyst is NaOH, KOH, NaOCH3, sulfuric acid or a sulfonic acid; more preferably, the chemical catalyst is sodium methoxide, NaOH and / or KOH. The amount of the chemical catalyst can be 0.1 to 1.0% of the total weight of the feedstock oil. Chemical catalysts can be used in forms well known in the art. For example, for sodium methoxide, it is usually added to the feedstock oil in solid form, and for NaOH and KOH, it is usually used in the form of an aqueous solution, and the concentration of an exemplary aqueous solution can be 30-50%. The amount described herein refers to the amount of the catalyst itself, not the amount of the solution. The reaction can be carried out at a temperature of 80-150°C, preferably 100-120°C. The reaction can be carried out under reduced pressure (e.g., under vacuum degree ≤ 10 mbar) for a period of time (e.g., 0.5 to 1 hour) to evenly distribute the fatty acids on the glycerol backbone. After the transesterification is completed, the reactants are washed with water.

[0067] When enzymatic transesterification is adopted, lipase can be used as a catalyst. As lipase, lipase powder or immobilized lipase fixed on a carrier (such as diatomaceous earth, ion exchange resin, etc.) can be used. The lipase preferably used is a lipase lacking site specificity, including but not limited to lipases derived from Alcaligenes and lipases derived from Candida. Suitable lipases include various commercially available immobilized enzymes or their fermentation broths. For example, Lipozyme TL IM and Lopozyme RM from Novozymes, and immobilized enzymes or their fermentation broths from AMANO Enzyme, Japan. The amount of lipase added is usually one ten-thousandth to ten ten-thousandths of the weight of the feedstock oil. According to the optimal reaction temperature of the lipase used, the reaction temperature of the pre-esterification can be in the range of 40-80°C, such as 70±5°C. Similarly, when the transesterification rate reaches 0.1-1.0%, the pre-esterification treatment is stopped. Depending on the specific reaction conditions, the reaction time of the enzymatic pre-esterification treatment may be in the range of 0.5-10 hours, such as 0.5-3 hours.

[0068] After the transesterification is completed, the obtained transesterified oil can be subjected to conventional refining, such as decolorization and deodorization.

[0069] The glyceride of odd-numbered fatty acids can be prepared by reacting odd-numbered fatty acids with glycerol. For example, an esterification reaction of odd-numbered fatty acids and glycerol can be carried out in the presence of lipase. Suitable lipases can be lipases commonly used in the art for esterification reactions, such as immobilized enzyme NOVO435 (Novozymes). Generally, the molar ratio of odd-numbered fatty acids to glycerol can be 2 to 5:1. The odd-numbered fatty acids used for the esterification reaction can be a mixture of several odd-numbered fatty acids or a single odd-numbered fatty acid. Generally, after mixing the odd-numbered fatty acids with glycerol, they are heated to 65 to 75°C, and then 1 to 20%, such as 5 to 15%, of the substrate weight of lipase is added, and the reaction is carried out under a vacuum degree of ≤10 mbar until the reaction is complete, and the glyceride of odd-numbered fatty acids used in the present invention can be obtained. The reaction can be carried out under stirring. The obtained glyceride of odd-numbered fatty acids can be purified by molecular distillation.

[0070] The edible oil for transesterification reaction can be various vegetable oils, microbial oils and animal oils well known in the art, including but not limited to: rice oil, sunflower oil (such as high oleic sunflower oil), rapeseed oil, palm oil, palm kernel oil, peanut oil, rapeseed oil, soybean oil, cottonseed oil, safflower seed oil, perilla seed oil, tea seed oil, olive oil, cocoa bean oil, Chinese tallow seed oil, almond oil, apricot oil, tung oil, rubber seed oil, corn oil, wheat germ oil, sesame seed oil, castor seed oil, evening primrose seed oil, hazelnut oil, pumpkin seed oil, walnut oil, grape seed oil, borage seed oil, sea buckthorn seed oil, tomato seed oil, macadamia nut oil, coconut oil and cocoa butter one or more. The animal oil is selected from one or more of lard, chicken fat, sheep fat, fish oil and butter. The microbial oil includes algae oil. The edible oil also includes the transesterification products and fractionation products of various oils, including but not limited to the various stearins obtained by fractionation, such as palm stearin. Suitable edible oil can be selected according to other effects desired to be obtained. For example, algae oil rich in DHA (docosahexaenoic acid) and / or vegetable oil rich in oleic acid, such as high oleic sunflower oil, may be selected. In some embodiments, the edible oil may also include palm stearin.

[0071] During the transesterification, the appropriate ratio of odd-numbered fatty acid triglycerides to vegetable oil can be selected according to the specific reaction conditions and the desired content of odd-numbered fatty acids in the oil. For example, in some embodiments, the weight ratio of odd-numbered fatty acid triglycerides to vegetable oil can be 45-70:30-55; in some embodiments, the weight ratio of odd-numbered fatty acid triglycerides to vegetable oil can be 50-65:35-50. In some embodiments, the weight ratio of odd-numbered fatty acid triglycerides to vegetable oil can be 55-62:38-45.

[0072] In some embodiments, the oil is a chemical ester exchange product of odd-numbered fatty acid triglycerides with DHA algae oil and high oleic sunflower oil; preferably, in the mixture of odd-numbered fatty acid triglycerides, DHA algae oil and high oleic sunflower oil, the weight ratio of pentadecanoic acid triglyceride to DHA algae oil and high oleic sunflower oil is 40-50:30-45:1-10, such as 40-50:30-40:5-10 or 40-50:38-45:1-5. In some embodiments, in the fatty acid composition of the oil, the content of C15:0 is 12-25%, preferably 16-22%, the content of C16:0 is 5-15%, preferably 10-15%, the content of C17:0 is 1-7%, preferably 2-5%, the content of C18:0 is 0.5-3%, preferably 1-2%, the content of C18:1 is 12-22%, preferably 15-20%, the content of C18:2 is 25-35%, preferably 30-35%, the content of C22:6 is 5-15%, preferably 7-12%; the content of other fatty acids is usually less than 1% or less than 0.5%.

[0073] In some embodiments, the oil is a chemical ester exchange product of odd-numbered carbon fatty acid triglyceride, palm stearin and high oleic sunflower oil; preferably, in the mixture of odd-numbered carbon fatty acid triglyceride, palm stearin and high oleic sunflower oil, the weight ratio of pentadecanoic acid triglyceride to palm stearin and high oleic sunflower oil is 55-62:1-5:35-40. In some embodiments, in the fatty acid composition of the oil, the content of C15:0 is 40-65%, preferably 50-60%, the content of C16:0 is 1-7%, preferably 3-5.5%, the content of C17:0 is 0.1-3%, preferably 0.1-1%, the content of C18:0 is 1-5%, preferably 1-3%, the content of C18:1 is 25-35%, preferably 28-34%, the content of C18:2 is 1-5%, preferably 2-4%; the content of the remaining fatty acids is usually less than 1% or less than 0.5%.

[0074] The use of odd-numbered fatty acids described herein includes one or more of the following odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preparations or drugs for one or more of the following items:

[0075] (1) increasing the protein expression abundance of tight junction-associated proteins (such as Occludin, Claudin and / or ZO-1) in a subject; in particular, increasing the protein expression abundance of the tight junction-associated proteins (such as Occludin, Claudin and / or ZO-1) in the intestine (such as intestinal mucosa), more specifically, the protein expression abundance of tight junction-associated proteins (such as Occludin, Claudin and / or ZO-1) in the duodenum, jejunum and ileum (such as their mucosa);

[0076] (2) reducing the level of corticotropin-releasing hormone (CRF) in the intestinal tissue of the subject; more preferably, reducing the level of corticotropin-releasing hormone (CRF) in the ileum tissue;

[0077] (3) Improve or enhance the intestinal mechanical barrier of the subject; improving the intestinal mechanical barrier can defend against the invasion of bacteria, toxins and foreign antigens, maintain the stability of the body's internal environment, and lay the foundation for the absorption of nutrients;

[0078] (4) increasing the level of immunoglobulins (such as IgG, IgA and / or IgM) in the intestinal tract of the subject; preferably, increasing the level of immunoglobulins (such as IgG, IgA and / or IgM) in the jejunum and ileum; more preferably, increasing the level of immunoglobulins IgG, IgA and / or IgM in the jejunum; more preferably, increasing the level of immunoglobulin A in the ileum;

[0079] (5) increasing the protein expression abundance of TLR4 and NF-κB in the intestinal tissues of the subjects, especially in the duodenum, jejunum, and ileum;

[0080] (6) maintaining homeostasis of inflammatory cytokines (such as TNF-α, IL-1β, IL-6, and / or IL-10) in the subject's ileum;

[0081] (7) increasing the expression of ileal mucin 2 in the subject;

[0082] (8) Increase the expression of HIF-1α in the intestine and promote the survival of intestinal cells in the intestinal hypoxic environment;

[0083] (9) Maintaining the immune homeostasis of the subject’s intestine (especially the ileum);

[0084] (10) increasing the content of nuclear protein Ki-67 in the intestinal tissue of the subject and promoting the proliferation of intestinal epithelial cells of the subject, preferably, the intestinal tissue is the duodenum, jejunum and / or ileum;

[0085] (11) activating the intestinal mTOR signaling pathway of the subject, increasing the expression of activated mTOR protein in intestinal cells (especially small intestinal cells, such as duodenum, jejunum, and ileum) and / or increasing the level of activated S6 kinase in intestinal cells (especially small intestinal cells, such as duodenum, jejunum, and ileum);

[0086] (12) increasing the level of digestive enzymes (including but not limited to maltase, aminopeptidase and / or sucrase) in the intestinal tract, especially the small intestine, of the subject, thereby promoting the absorption of nutrients;

[0087] (13) increasing the level of serotonin in the intestinal tissues (especially the duodenum, jejunum and / or ileum) of the subject and the content of substance P (a neuropeptide) in the ileum, and enhancing the function of the small intestine, such as increasing intestinal motility, promoting gastrointestinal smooth muscle contraction, inhibiting gastric acid and bile secretion, and regulating local gastrointestinal blood flow;

[0088] (14) promoting intestinal development of a subject;

[0089] (15) down-regulating the expression of mitophagy-related proteins (such as ULK1, TFEB and / or Parkin) in the intestinal tissue cells (especially the duodenum, jejunum and / or ileum) of the subject to alleviate mitochondrial dysfunction;

[0090] (16) up-regulating the level of lipid synthesis-related transcription factors (such as PPARγ and / or SREBP-1) in the subject's intestine (especially the small intestine, especially the duodenum and jejunum), and improving the absorption and anabolism of lipids in the intestine (especially the small intestine, especially the duodenum and jejunum);

[0091] (17) Maintaining energy homeostasis of intestinal cells and improving intestinal energy metabolism;

[0092] (18) Upregulate the content of type I and type II muscle fibers and the expression of mTOR protein in the muscle tissue of the subjects, while reducing the relative content of AMPK and PGC1-α;

[0093] (19) improving the energy status of the subject's muscle tissue, promoting cell growth and development, increasing muscle fiber content, inhibiting the conversion of type II muscle fibers to type I muscle fibers, increasing muscle mass, and promoting the overall development of muscle tissue;

[0094] (20) Upregulating the expression of SREBP-1 in the subject's muscle tissue, promoting lipid anabolism, increasing the uptake and utilization of lipids by muscle tissue, improving energy status, and promoting the development and metabolism of muscle tissue;

[0095] (21) promoting the development and metabolism of muscle tissue of a subject;

[0096] (22) Upregulate the expression of activated mTOR in the subject, reduce the expression of Prdm16 and Irisin, inhibit lipolysis, and increase lipid synthesis to promote the development of adipose tissue;

[0097] (23) Upregulate the levels of SERBP-1 and APOB in the subject’s adipose tissue, increase lipid synthesis in adipose tissue, enhance the body’s transport of lipids, and maintain the energy balance between adipose tissue and the body;

[0098] (24) promoting the development and metabolism of adipose tissue in a subject;

[0099] (25) Upregulate the level of GSH-PX in the subject’s serum, improve the body’s overall antioxidant capacity, and maintain overall redox balance;

[0100] (26) reducing the levels of HIS, jejunal IgE, ileal IgE, jejunal HIS, and ileal HIS in the subject's blood, and reducing the allergic reactions of the body and the jejunum and ileum;

[0101] (27) reducing allergic reactions in the subject’s body and intestines;

[0102] (28) Reduce insulin resistance during pregnancy;

[0103] (29) Control the subject’s blood sugar during pregnancy;

[0104] (30) Improve insulin resistance caused by poor diet (such as low-protein diet);

[0105] (31) Prevent gestational diabetes, as well as macrosomia, fetal malformation, premature birth, premature rupture of membranes and / or polyhydramnios caused by gestational diabetes, and reduce fetal mortality;

[0106] (32) reduce serum bile acid levels during pregnancy;

[0107] (33) Prevent or improve intrahepatic cholestasis of pregnancy in a subject, such as intrahepatic cholestasis of pregnancy caused by poor diet or disease; reduce the occurrence or risk of fetal distress, premature birth, and perinatal mortality in a subject with intrahepatic cholestasis of pregnancy;

[0108] (34) increasing the level of superoxide dismutase and glutathione peroxidase in the subject's liver, decreasing the level of malondialdehyde in the subject's liver, and decreasing oxidative stress in the subject during pregnancy;

[0109] (35) Improving the pathological damage of intestinal tissue induced by abnormal diet or disease;

[0110] (36) reduce the subject's colon inflammatory factors (such as IL-1β, IL-6, TNF-α, NLRP3 and / or GSDMD) and alleviate intestinal inflammation;

[0111] (37) Treatment or prevention of inflammatory bowel disease and colorectal cancer;

[0112] (38) reducing the abundance of Helicobacter pylori and / or Deferribacter in the subject and improving the intestinal microecology; and

[0113] (39) Preventing or treating diseases caused by Helicobacter pylori, including gastric cancer.

[0114] In some embodiments, the use of odd-numbered fatty acids described herein includes the following uses of odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preparations or drugs for the following purposes:

[0115] (1) increasing the protein expression abundance of tight junction-associated proteins (such as occludin, claudin and / or ZO-1) in a subject; in particular, increasing the protein expression abundance of the tight junction-associated proteins (such as occludin, claudin and / or ZO-1) in the intestine (such as intestinal mucosa), more specifically, the protein expression abundance of tight junction-associated proteins (such as occludin, claudin and / or ZO-1) in the duodenum, jejunum and ileum (such as their mucosa); and

[0116] (2) reducing the level of corticotropin-releasing hormone (CRF) in the intestinal tissue of the subjects;

[0117] Thereby improving or enhancing the intestinal mechanical barrier of the subject.

[0118] In some embodiments, the use of odd-numbered fatty acids described herein includes the following uses of odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preparations or drugs for one or more of the following items:

[0119] (4) increasing the level of immunoglobulins (such as IgG, IgA and / or IgM) in the intestinal tract of the subject; preferably, increasing the level of immunoglobulins (such as IgG, IgA and / or IgM) in the jejunum and ileum; more preferably, increasing the level of immunoglobulins IgG, IgA and / or IgM in the jejunum, and increasing the level of immunoglobulin A in the ileum;

[0120] (5) increasing the protein expression abundance of TLR4 and NF-κB in the intestinal tissues of the subjects, especially in the duodenum, jejunum, and ileum;

[0121] (6) maintaining homeostasis of inflammatory cytokines (such as TNF-α, IL-1β, IL-6, and / or IL-10) in the subject's ileum;

[0122] (7) increasing the expression of ileal mucin 2 in the subject; and

[0123] (8) Increase the expression of HIF-1α in the intestine and promote the survival of intestinal cells in the intestinal hypoxic environment;

[0124] (9) Maintain the immune homeostasis of the subject’s intestine (especially the ileum).

[0125] In some embodiments, the use of odd-numbered fatty acids described herein includes the following uses of odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preparations or drugs for one or more of the following items:

[0126] (10) increasing the content of nuclear protein Ki-67 in the intestinal tissue of the subject and promoting the proliferation of intestinal epithelial cells of the subject; preferably, the intestinal tissue is the duodenum, jejunum and / or ileum;

[0127] (11) activating the intestinal mTOR signaling pathway of the subject, increasing the expression of activated mTOR protein in intestinal cells (especially small intestinal cells) and / or increasing the level of activated S6 kinase in intestinal cells (especially small intestinal cells);

[0128] (12) increasing the level of digestive enzymes (including but not limited to maltase, aminopeptidase and / or sucrase) in the intestinal tract, especially the small intestine, of the subject to promote the absorption of nutrients; and

[0129] (13) increasing the level of 5-HT in the intestinal tissues (especially the duodenum, jejunum and / or ileum) and the content of substance P in the ileum, and enhancing the function of the small intestine, such as increasing intestinal motility, promoting gastrointestinal smooth muscle contraction, inhibiting gastric acid and bile secretion, and regulating local gastrointestinal blood flow;

[0130] Thereby promoting the intestinal development of the subject.

[0131] In some embodiments, the use of odd-numbered fatty acids described herein includes the following uses of odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preparations or drugs for one or more of the following items:

[0132] (15) down-regulating the expression of mitophagy-related proteins (such as ULK1, TFEB and / or Parkin) in the intestinal tissue cells of the subject to alleviate mitochondrial dysfunction; and / or

[0133] (16) upregulating the levels of transcription factors related to lipid synthesis (such as PPARγ and / or SREBP-1) in the subject's intestine (especially the small intestine), and improving the absorption and anabolism of lipids in the intestine (especially the small intestine, especially the duodenum and jejunum);

[0134] Thereby maintaining the energy homeostasis of the subject's intestinal cells and improving intestinal energy metabolism.

[0135] In some embodiments, the use of odd-numbered fatty acids described herein includes the following uses of odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preparations or drugs for one or more of the following items:

[0136] (18) upregulating the content of type I and type II muscle fibers and the expression of mTOR protein in the muscle tissue of the subject, while reducing the relative content of AMPK and PGC1-α; and / or

[0137] (19) improving the energy status of the subject's muscle tissue, promoting cell proliferation and tissue development, increasing muscle fiber content, inhibiting the conversion of type II muscle fibers to type I muscle fibers, increasing muscle mass, and promoting the overall development of muscle tissue; and / or

[0138] (20) Upregulating the expression of SREBP-1 in the subject's muscle tissue, promoting lipid anabolism, increasing the uptake and utilization of lipids by muscle tissue, improving energy status, and promoting the development and metabolism of muscle tissue;

[0139] Thereby promoting the development and metabolism of the subject's muscle tissue.

[0140] In some embodiments, the use of odd-numbered fatty acids described herein includes the following uses of odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preparations or drugs for one or more of the following items:

[0141] (22) upregulating the expression of activated mTOR in the subject, reducing the expression of Prdm16 and Irisin, inhibiting lipolysis, and increasing lipid synthesis to promote the development of adipose tissue; and / or

[0142] (23) Upregulate the levels of SERBP-1 and APOB in the subject’s adipose tissue, increase lipid synthesis in adipose tissue, enhance the body’s transport of lipids, and maintain the energy balance between adipose tissue and the body;

[0143] Thereby promoting the development and metabolism of the subject's adipose tissue.

[0144] In some embodiments, the use of odd-numbered fatty acids described herein includes the following uses of odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preparations or drugs for one or more of the following items:

[0145] (25) upregulating the level of GSH-PX in the subject's serum, improving the body's overall antioxidant capacity, and maintaining overall redox balance; and / or

[0146] (26) reducing the levels of HIS, jejunal IgE, ileal IgE, jejunal HIS, and ileal HIS in the subject's blood, and reducing the allergic reactions of the body and the jejunum and ileum;

[0147] Thereby reducing the allergic reaction of the subject's body and intestines.

[0148] In some embodiments, the use of odd-numbered fatty acids described herein includes the following uses of odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preparations or drugs for one or more of the following items:

[0149] (28) reducing insulin resistance during pregnancy; and / or

[0150] (29) Control the subject’s blood sugar during pregnancy;

[0151] This can prevent gestational diabetes, as well as macrosomia, fetal malformations, premature birth, premature rupture of membranes and / or polyhydramnios caused by gestational diabetes, and reduce fetal mortality.

[0152] In some embodiments, the use of odd-numbered fatty acids described herein includes the following uses of odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preparations or drugs for the following purposes: reducing the serum bile acid level of the subject during pregnancy, thereby preventing or improving the subject's intrahepatic cholestasis of pregnancy, such as intrahepatic cholestasis of pregnancy caused by poor diet or disease. In some embodiments, the use of odd-numbered fatty acids described herein includes the following uses of odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preparations or drugs for the following purposes: reducing the occurrence or risk of fetal distress, premature birth, and perinatal mortality in the subject's intrahepatic cholestasis of pregnancy.

[0153] In some embodiments, the use of odd-numbered fatty acids described herein includes the following uses of odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preparations or drugs for the following purposes: increasing the level of superoxide dismutase and glutathione peroxidase in the liver of a subject, reducing the level of malondialdehyde in the liver of a subject, reducing oxidative stress in a subject during pregnancy, thereby improving the pathological damage to intestinal tissue induced by abnormal diet or disease in the subject.

[0154] In some embodiments, the uses of odd-numbered fatty acids described herein include the following uses of odd-numbered fatty acids, and also include the use of odd-numbered fatty acids in the preparation of preparations or drugs for the following purposes: reducing colon inflammatory factors in a subject, thereby treating or preventing inflammatory bowel disease and colorectal cancer.

[0155] In some embodiments, the uses of odd-numbered fatty acids described herein include the following uses of odd-numbered fatty acids, and also include the use of odd-numbered fatty acids in the preparation of preparations or drugs for the following purposes: reducing Helicobacter pylori in a subject, thereby preventing or treating a disease caused by Helicobacter pylori bacteria in the subject, including gastric cancer.

[0156] In some embodiments, the use of odd-numbered fatty acids described herein includes the following uses of odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preparations or drugs for the following purposes:

[0157] Improve or enhance the intestinal mechanical barrier of the subject, maintain the immune homeostasis of the subject's intestine (especially the ileum), promote the development of the subject's intestine, maintain the energy homeostasis of the subject's intestinal cells, and improve intestinal energy metabolism; and / or

[0158] Promoting the development and metabolism of a subject's muscle tissue; and / or

[0159] Promoting the development and metabolism of adipose tissue in a subject; and / or

[0160] Reduces allergic reactions in the subject's body and intestines.

[0161] In some embodiments, the use of odd-numbered fatty acids described herein includes the following uses of odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preparations or drugs for the following purposes:

[0162] Improve intestinal health, preferably, the improvement of intestinal health is to enhance intestinal mechanical barrier function, enhance intestinal immune homeostasis, promote intestinal development, increase intestinal digestive enzyme levels, enhance nutrient absorption, maintain intestinal cell energy homeostasis, improve intestinal tissue pathological damage, relieve intestinal inflammation and / or improve intestinal microecology; and / or

[0163] Improve muscle tissue development and metabolism; and / or

[0164] Improve adipose tissue development and metabolism; and / or

[0165] Improve antioxidant capacity or reduce oxidative stress; and / or

[0166] Reducing allergic reactions, preferably reducing intestinal allergic reactions; and / or

[0167] Improve insulin resistance caused by a low-protein diet; and / or

[0168] Improve bile acid metabolism.

[0169] In some embodiments, the use of odd-numbered fatty acids described herein includes the following uses of odd-numbered fatty acids, and also includes the use of odd-numbered fatty acids in the preparation of preventive, therapeutic or adjuvant therapeutic agents for at least one of the following diseases or conditions: inflammatory bowel disease, colorectal cancer, diarrhea, irritable bowel syndrome, intestinal ulcers, intestinal allergies, intestinal dysbiosis, Helicobacter pylori infection, gestational diabetes (especially for gestational diabetes patients with a low-protein diet or accompanied by a low-protein diet) and intrahepatic cholestasis (especially intrahepatic cholestasis of pregnancy).

[0170] In some embodiments, the following methods are also provided herein:

[0171] (1) A method for increasing the protein expression abundance of a tight junction-associated protein (such as occludin, claudin and / or ZO-1) in a subject; in particular, a method for increasing the protein expression abundance of the tight junction-associated protein (such as occludin, claudin and / or ZO-1) in the intestine (such as intestinal mucosa), more specifically, a method for increasing the protein expression abundance of the tight junction-associated protein (such as occludin, claudin and / or ZO-1) in the duodenum, jejunum and ileum (such as their mucosa);

[0172] (2) A method for reducing the level of corticotropin-releasing hormone (CRF) in the intestinal tissue of a subject; more preferably, a method for reducing the level of corticotropin-releasing hormone (CRF) in the ileum tissue;

[0173] (3) methods for improving or enhancing the intestinal mechanical barrier of a subject;

[0174] (4) A method for increasing the content of immunoglobulins (such as IgG, IgA and / or IgM) in the intestinal tract of a subject; preferably, a method for increasing the content of immunoglobulins (such as IgG, IgA and / or IgM) in the jejunum and ileum; more preferably, a method for increasing the content of immunoglobulins IgG, IgA and / or IgM in the jejunum; more preferably, a method for increasing the content of immunoglobulin A in the ileum;

[0175] (5) A method for increasing the protein expression abundance of TLR4 and NF-κB in the intestinal tissues of a subject, particularly in the duodenum, jejunum, and ileum;

[0176] (6) Methods for maintaining homeostasis of inflammatory cytokines (such as TNF-α, IL-1β, IL-6 and / or IL-10) in the ileum of a subject;

[0177] (7) A method for increasing the expression of ileal mucin 2 in a subject;

[0178] (8) Methods for increasing the expression of HIF-1α in the intestine and promoting the survival of intestinal cells in the intestinal hypoxic environment;

[0179] (9) Methods for maintaining immune homeostasis in the intestine (especially the ileum) of a subject;

[0180] (10) A method for increasing the content of nuclear protein Ki-67 in the intestinal tissue of a subject, preferably, the intestinal tissue is the duodenum, jejunum and / or ileum; a method for promoting the proliferation of intestinal epithelial cells of a subject;

[0181] (11) A method for activating the intestinal mTOR signaling pathway of a subject, increasing the expression of activated mTOR protein in intestinal cells (especially intestinal cells such as the duodenum, jejunum, and ileum) and / or increasing the level of activated S6 kinase in intestinal cells (especially intestinal cells such as the duodenum, jejunum, and ileum);

[0182] (12) A method for increasing the level of digestive enzymes (including but not limited to maltase, aminopeptidase and / or sucrase) in the intestinal tract, especially the small intestine, of a subject to promote the absorption of nutrients;

[0183] (13) Methods for increasing the level of serotonin in the intestinal tissues (especially the duodenum, jejunum and / or ileum) of a subject and the content of substance P (a neuropeptide) in the ileum, and enhancing the function of the small intestine, such as increasing intestinal motility, promoting gastrointestinal smooth muscle contraction, inhibiting gastric acid and bile secretion, and regulating local gastrointestinal blood flow;

[0184] (14) Methods for promoting intestinal development in a subject;

[0185] (15) A method for alleviating mitochondrial dysfunction by down-regulating the expression of mitophagy-related proteins (such as ULK1, TFEB and / or Parkin) in the intestinal tissue cells (especially the duodenum, jejunum and / or ileum) of the subject;

[0186] (16) A method for upregulating the level of lipid synthesis-related transcription factors (such as PPARγ and / or SREBP-1) in the intestinal tract (especially the small intestine, especially the duodenum and jejunum) of a subject, thereby improving the absorption and anabolism of lipids in the intestinal tract (especially the small intestine, especially the duodenum and jejunum);

[0187] (17) Methods for maintaining energy homeostasis in intestinal cells of a subject and improving intestinal energy metabolism;

[0188] (18) A method for upregulating the content of type I and type II muscle fibers and the expression of mTOR protein in the muscle tissue of a subject, while reducing the relative content of AMPK and PGC1-α;

[0189] (19) A method for improving the energy status of a subject's muscle tissue, promoting cell growth and development, increasing muscle fiber content, inhibiting the conversion of type II muscle fibers to type I muscle fibers, increasing muscle mass, and promoting the overall development of muscle tissue;

[0190] (20) A method for upregulating the expression of SREBP-1 in the muscle tissue of a subject, promoting lipid anabolism, increasing the uptake and utilization of lipids by muscle tissue, improving energy status, and promoting the development and metabolism of muscle tissue;

[0191] (21) Methods for promoting the development and metabolism of muscle tissue in a subject;

[0192] (22) a method for upregulating the expression of activated mTOR in a subject, reducing the expression of Prdm16 and Irisin, inhibiting lipolysis, and increasing lipid synthesis to promote the development of adipose tissue;

[0193] (23) A method for upregulating the levels of SERBP-1 and APOB in adipose tissue of a subject, increasing lipid synthesis in adipose tissue, enhancing lipid transport by the body, and maintaining energy balance between adipose tissue and the body;

[0194] (24) Methods for promoting the development and metabolism of adipose tissue in a subject;

[0195] (25) A method for increasing the level of GSH-PX in the serum of a subject, improving the overall antioxidant capacity of the body, and maintaining the overall redox balance;

[0196] (26) A method for reducing the levels of HIS, jejunal IgE, ileal IgE, jejunal HIS, and ileal HIS in a subject's blood, thereby reducing allergic reactions in the body and the jejunum and ileum;

[0197] (27) Methods for reducing allergic reactions in the body and intestines of a subject;

[0198] (28) Methods for reducing insulin resistance during pregnancy in a subject;

[0199] (29) Methods for controlling blood sugar during pregnancy;

[0200] (30) Methods to improve insulin resistance caused by poor diet (such as low-protein diet);

[0201] (31) Methods for preventing gestational diabetes mellitus, as well as methods for preventing fetal macrosomia, fetal malformation, premature birth, premature rupture of membranes and / or polyhydramnios caused by gestational diabetes mellitus, and reducing fetal mortality;

[0202] (32) A method for reducing serum bile acid levels in a subject during pregnancy;

[0203] (33) Methods for preventing or ameliorating intrahepatic cholestasis of pregnancy in a subject, such as intrahepatic cholestasis of pregnancy caused by poor diet or disease; methods for reducing the occurrence or risk of fetal distress, premature birth, and perinatal mortality in a subject with intrahepatic cholestasis of pregnancy;

[0204] (34) A method for increasing the level of superoxide dismutase and glutathione peroxidase in a subject's liver, decreasing the level of malondialdehyde in a subject's liver, and decreasing oxidative stress in a subject during pregnancy;

[0205] (35) A method for improving the pathological damage to intestinal tissue induced by abnormal diet or disease in a subject;

[0206] (36) A method for reducing colon inflammatory factors (such as IL-1β, IL-6, TNF-α, NLRP3 and / or GSDMD) in a subject to alleviate intestinal inflammation;

[0207] (37) Methods for treating or preventing inflammatory bowel disease and colorectal cancer;

[0208] (38) A method for reducing the abundance of Helicobacter pylori and / or Deferribacter in a subject and improving the intestinal microecology; and

[0209] (39) Methods for preventing or treating diseases caused by Helicobacter pylori, including gastric cancer;

[0210] Each of the methods comprises administering to a subject in need thereof an effective amount of an odd-numbered fatty acid. The odd-numbered fatty acid is as described in any embodiment herein. It should be understood that the odd-numbered fatty acid can be provided in a free form, in the form of a glyceride (such as a monoglyceride, a diglyceride and / or a triglyceride) of the odd-numbered fatty acid, or in the form of a fat (such as a fat described herein).

[0211] In some embodiments of the uses and methods described herein, the oil has the following fatty acid composition: C15:0 content is 50-60%, preferably 55-60%, C16:0 content is 1-7%, preferably 3-5.5%, C17:0 content is 0.1-3%, preferably 0.1-1%, C18:0 content is 1-5%, preferably 1-3%, C18:1 content is 25-35%, preferably 28-34%, C18:2 content is 1-5%, preferably 2-4%; the content of other fatty acids is generally less than 1% or less than 0.5%. In some embodiments, the oil is a chemical ester exchange product of odd-numbered fatty acid triglycerides with palm stearin and high oleic sunflower oil; preferably, in the mixture of odd-numbered fatty acid triglycerides, palm stearin and high oleic sunflower oil, the weight ratio of pentadecanoic acid triglyceride to palm stearin and high oleic sunflower oil is 55-62:1-5:35-40.Preferably, the application and method include one or more of the following items: increasing the protein expression abundance of tight junction-associated proteins (such as Occludin, Claudin and ZO-1) in the mucosa of the duodenum, jejunum and ileum; reducing the content of CRF in intestinal tissue; enhancing or improving the mechanical barrier of the intestine of piglets; increasing the levels of IgG, IgA and IgM in the jejunum; increasing the level of IgA in the ileum; upregulating the protein expression abundance of TLR4 and NF-κB in the duodenum, jejunum and ileum; regulating inflammatory cytokines (such as TNF-α, IL-1β, IL-6 and / or IL-10) to maintain ileal immune homeostasis; maintaining the level of mucin in the intestinal mucosa and maintaining the immune homeostasis of the ileum; improving intestinal epithelial cells It can also reduce the protein expression abundance of Ki67 in the small intestine, promote intestinal epithelial cell proliferation, improve intestinal mechanical barrier and promote intestinal development; activate the mTOR signaling pathway, increase the expression of activated mTOR protein in small intestinal cells, promote cell growth and tissue development; increase the level of activated S6 kinase in small intestinal cells, rescue cell proliferation and protein metabolism in small intestinal tissue, and promote tissue development; increase the level of small intestinal digestive enzymes (including maltase, aminopeptidase and / or sucrase), and promote the absorption of nutrients; increase the level of serotonin in the duodenum, jejunum and ileum and the content of substance P in the ileum, regulate intestinal peristalsis, promote gastrointestinal smooth muscle contraction, inhibit gastric acid and bile secretion, regulate local gastrointestinal blood flow, and enhance the function of the small intestine; downregulate intracellular mitochondria It can reduce the expression of autophagy-related proteins (including ULK1, TFEB and / or Parkin), alleviate mitochondrial dysfunction, and maintain the energy homeostasis of intestinal cells; upregulate the levels of lipid synthesis-related transcription factors (including PPARγ and / or SREBP-1), improve the absorption and anabolism of lipids in the small intestine, and maintain the energy homeostasis of intestinal cells; upregulate the content of type I and type II muscle fibers and the expression of mTOR protein in muscle tissue, reduce the relative content of AMPK and PGC1-α, alleviate the energy state of muscle tissue, promote cell proliferation and tissue development, increase muscle fiber content, inhibit the transformation of type II muscle fibers to type I muscle fibers, increase muscle mass, and promote the overall development of muscle tissue; upregulate SRE in muscle tissue It reduces the expression of BP-1, increases the uptake and utilization of lipids by muscle tissue, improves energy status, and promotes the development of muscle tissue; it upregulates the expression of activated mTOR and reduces the expression of Prdm16 and Irisin, which inhibits lipolysis, increases lipid synthesis, and promotes the development of adipose tissue; it upregulates the level of SERBP-1 in adipose tissue, maintains the level of APOB, improves lipid synthesis in adipose tissue, strengthens the body's transport of lipids, and maintains the energy balance of adipose tissue and the body; it maintains the content of GSH-PX in serum, improves the body's overall antioxidant capacity, and maintains the overall redox balance; it reduces blood HIS, jejunal IgE, ileal IgE and HIS, and reduces allergic reactions of the body and the jejunum and ileum.

[0212] Herein, "individual" or "subject" mainly refers to mammals, such as humans, farmed livestock (such as pigs, cattle, sheep, horses, camels, donkeys, etc.), research mammals (such as rats, mice, gorillas, monkeys, dogs, etc.), artificially raised animals or wild animals, etc. This application also does not exclude individuals other than mammals, such as poultry, aquatic species, etc.

[0213] Herein, an effective amount refers to an amount that can achieve the desired purpose by taking it for a period of time. A person skilled in the art can determine the effective amount using conventional methods in the art according to different individuals, different purposes or symptoms.

[0214] The preparations described herein may be food or, for example, dietary supplements. Dietary supplements may contain other ingredients contained in conventional dietary supplements, such as dietary fiber, vitamins, minerals, etc. Dietary supplements may be provided in the form of, for example, capsules, granules, powders, tablets, drops, blocks, or capsules, or pills, or semi-emulsions or emulsions. The food may be a beverage, dairy product, candy, chocolate, cake, snack food, meat product, egg product, cold food, pet food, feed. The dairy product may be milk powder, liquid milk, milk tablets, yogurt, etc.; the cake may be biscuits, bread, cake, etc.; the beverage may be a carbonated beverage, soda, fruit-flavored water, sour plum soup, bulk low-sugar beverage, mineral beverage, malted milk, milk tea, coffee, etc.; the cold food may be popsicles, ice cream, ice cream, pudding, etc.

[0215] The drugs described herein, in addition to the odd-numbered fatty acids described herein, may also contain pharmaceutically acceptable carriers well known in the art.

[0216] The present invention will be further described below in conjunction with specific examples. It should be understood that these examples are only used to illustrate the present invention and are not intended to limit the scope of the present invention. The experimental methods in the following examples without specifying specific conditions are usually based on conventional conditions or the conditions recommended by the manufacturer. Unless otherwise stated, percentages and parts are calculated by weight.

[0217] Example 1

[0218] 1. Basic process of the experiment

[0219] After mixing the oils in the table below, chemical transesterification is performed to evenly distribute the fatty acids on the glycerol backbone, eliminating the digestion, absorption and functional effects caused by the difference in the position of fatty acids. The obtained oil is refined to make an oil-in-water emulsion. The oil-in-water emulsion is spray-dried to make oil powder. The oil powder is fed to piglets as a dietary supplement.

[0220] Grease 1 Hard ST: high oleic sunflower oil = 73:27 Grease 2 OCFA algae oil: high oleic acid sunflower oil = 92:8 Grease 3 C15-TAG: Hard ST: High Oleic Sunflower Oil = 59:4:37

[0221] The feeding method of piglets is that the piglets are weaned at 7 days old and fed with commercial formula milk powder for 6 days. Then, fat powder is added to the first milk of the piglets every day to dissolve the fat powder and then feed the piglets. The piglets are fed with commercial formula milk powder normally at other times for a total of 15 days.

[0222] 2. Preparation of odd-numbered fatty acid triglycerides

[0223] Glycerol (Yihai Jiali) and pentadecanoic acid (Adamas, purity ≥ 95%) were mixed in a molar ratio of 1:4, heated to 70°C and mixed evenly as a reaction substrate, and 10% of the substrate weight of immobilized enzyme NOVO435 (Novozymes) was added, and the reaction was carried out at 70°C, 300rpm, and vacuum degree ≤ 10mbar for 15h to obtain a crude oil product. The obtained crude oil product was separated by molecular distillation, and the heavy phase was pentadecanoic acid glyceride (C15-TAG) with a purity of > 98%.

[0224] The above method was adopted to prepare undecanoic acid triglyceride, tridecanoic acid triglyceride and heptadecanoic acid triglyceride using undecanoic acid (Adamas, purity ≥ 99%), tridecanoic acid (Shaoyuan, purity ≥ 95%) and heptadecanoic acid (Adamas, purity ≥ 98%) respectively.

[0225] 3. Oil Preparation

[0226] Grease 1

[0227] Hard ST (Yihai Kerry, batch RBDHard ST 321, acid value 0.04mg / KOH / g) and high oleic sunflower oil (Yihai Kerry, model finished product level 1) were melted and mixed uniformly in a mass ratio of 73:27, and then chemical ester exchange was performed to make the fatty acids evenly distributed on the glycerol skeleton. The process of chemical ester exchange is: first vacuum dehydration at 110°C for 1h, then adding sodium methoxide with a weight of 0.2% of the oil, vacuum reaction at 110°C for 1h, cooling to below 80°C, adding citric acid with a mass of 1.8 times that of sodium methoxide (to make a 10% citric acid solution), stirring and pouring into a separatory funnel, washing with hot water until neutral, and then vacuum dehydration at 110°C. The above-mentioned obtained oil can be refined according to conventional oil refining methods. This embodiment adopts the following oil refining method for refining to obtain oil 1.

[0228] Oil refining method:

[0229] 1. Weigh 500g of oil into a 2L glass jacketed reactor and heat it naturally until it melts and keep it at 60°C. Stir at 200rpm. Fill with nitrogen for protection throughout the process. Detect AV (acid value) and PV (peroxide value).

[0230] 2. Wash with water, gradually add citric acid solution (water addition amount is 15%, citric acid addition amount is 0.5‰), stir at 200rpm for 5min, stop stirring, let it stand for 4h, and put down the water phase after the sedimentation is completed. Then gradually add water (water addition amount is 15%), stir at 200rpm for 5min, then stop stirring, let it stand for 4h; after the sedimentation is completed, put down the water phase.

[0231] 3. Alkali refining, sampling and testing AV and PV, calculate the amount of alkali added, the amount of alkali added = theoretical alkali (0.713 × oil weight (ton) × acid value / 0.93 alkali concentration) + excess alkali (crude oil weight * 0.0005), water added (kg) = alkali added (kg) × 40; prepare alkali solution with water and alkali; heat the oil to 60°C; turn on the stirring at 100rpm, then add the alkali solution within 5min, stir quickly for 5min after adding, and let it settle for 4-6h; after settling, discharge the lower aqueous phase; brine washing: add 15% water and 0.5‰ salt, gradually add them dropwise to the algae oil, stir at 100rpm, turn off the stirring after stirring for 3min, settle for 3h, and discharge the lower aqueous phase after settling. Alkaline water washing: 15% water and 0.2‰ alkali are gradually added to the oil, stirring at 100rpm, stirring for 3 minutes, then turning off the stirring, settling for 3 hours, and releasing the lower aqueous phase after the settling is completed. Repeat the alkaline water washing twice. Water washing: 15% water is added, stirring for 3 minutes after addition, then turning off the stirring, settling for 3 hours, and releasing the lower aqueous phase after the settling is completed. Wash twice in total.

[0232] 4. Decolorization: decolorization and deodorization are carried out according to conventional methods. The decolorization temperature is 105°C, and about 2% of the oil weight of white clay is added as a decolorization adsorbent. The vacuum degree is 10mbar, and the decolorization is carried out for 0.5h before filtering;

[0233] 5. Deodorization, temperature is 200℃, vacuum degree is 5mbar, nitrogen is passed, deodorization time is 2h, and refined oil is obtained after refining.

[0234] Grease 2

[0235] OCFA algae oil (Yihai Kerry) and high oleic sunflower oil (Yihai Kerry) were melted and mixed evenly in a mass ratio of 92:8, and then chemically transesterified to make the fatty acids evenly distributed on the glycerol backbone, and then the resulting oil was refined. The chemical transesterification and oil refining methods are the same as those of Oil 1 (the animal test in this application uses the oil obtained by this preparation method).

[0236] Oil 2 can also be prepared according to the following method: the undecanoic acid triglyceride, tridecanoic acid triglyceride, pentadecanoic acid triglyceride, and heptadecanoic acid triglyceride prepared according to the method described above are melted and mixed evenly with DHA algae oil (obtained by refining crude oil purchased from Qingdao Keyuan, and the refining method refers to "Optimization of Huanghuai New Microalgae DHA Refining Process", crude oil batch MKD120056) and high oleic sunflower oil (Yihai Kerry) at a mass ratio of 1:3:47:7:35:7, and then chemically transesterified to evenly distribute fatty acids on the glycerol skeleton, and then the obtained oil is refined. The chemical transesterification and oil refining methods are the same as those of oil 1.

[0237] Grease 3 :

[0238] C15-TAG, Hard ST (Yihai Kerry) and high oleic sunflower oil (Yihai Kerry) were melted and mixed evenly in a mass ratio of 59:4:37, and then chemically transesterified to make the fatty acids evenly distributed on the glycerol backbone. The chemical transesterification and oil refining methods were the same as those of oil 1.

[0239] The Hard ST and high oleic sunflower oil used in the above oils 1-3 are products of the same batch from the same manufacturer.

[0240] 4. Fatty acid composition of oil

[0241] The main fatty acid compositions of the above Hard ST, high oleic sunflower oil, DHA algae oil and OCFA algae oil as well as the main fatty acid compositions of oils 1 to 3 were tested with reference to the third method “normalization method” in “GB5009.168-2016 National Food Safety Standard Determination of Fatty Acids in Food”. The results are shown in Tables 1-1 and 1-2, respectively.

[0242] Table 1-1: Main fatty acid composition of Hard ST, high oleic sunflower oil, DHA algae oil and OCFA algae oil

[0243]

[0244]

[0245] Table 1-2: Major fatty acid composition of oils 1-3

[0246]

[0247]

[0248] 5. Preparation of lipid dietary supplement

[0249] 15 g of monoglyceride (Yihai Kerry, model DMG-CF01), 15 g of phospholipid (Yihai Kerry, non-GMO soybean lecithin) and 300 g of oil (i.e., the above oils 1, 2, and 3) were mixed, stirred at 60°C until dissolved and mixed evenly, 1.08 kg of lactose and 97.5 g of sodium caseinate were added to the aqueous solution obtained by dissolving in 3.5 kg of pure water, high-speed shearing was performed at 12000 rpm for 8 minutes, and high-pressure homogenization was performed twice at a pressure of 300 bar to complete the preparation of the emulsion. The above emulsion was spray-dried at an inlet temperature of 180°C and an outlet temperature of 90°C to obtain oil dietary supplements 1-3. The oils used in oil dietary supplements 1-3 are shown in Table 2 below.

[0250] Table 2: Fats and oils used in dietary supplements

[0251] Dietary Supplements Grease used Oil dietary supplement1 Grease 1 Oil dietary supplement2 Grease 2 Oil dietary supplement3 Grease 3

[0252] 6. Animal Experiments

[0253] Experimental animals: The experiment selected healthy 7-day-old "Du×Chang×Da" weaned piglets, and divided them into 3 groups (see Table 3) according to the principle of similar weight, gender and genetic background, with 10 pigs in each group; another pig farm-raised homologous piglet breastfeeding group G0 group was set up, with 10 pigs in each group. The 7-day-old piglets were transferred from the pig farm to the Institute of Subtropical Medicine, Chinese Academy of Sciences, and fed with commercial piglet formula milk powder (Tangrenshen) and adapted to the environment; daily management was carried out according to the large-scale pig farm management model. After 6 days of pre-feeding, the dietary supplements mentioned above were added to the basic formula milk powder (Tangrenshen) in the first meal of the day, and they were fed to 28 days of age, fasted for 12 hours, and then slaughtered for sampling. Samples of 8 piglets were collected from each group for detection and analysis. All relevant operation procedures were in accordance with the requirements of the Animal Welfare and Animal Experiment Ethics Committee of the Institute of Subtropical Medicine, Chinese Academy of Sciences.

[0254] Table 3: Experimental treatment groups

[0255] Grouping Daily Diet Number of animals Control group (G0) Breast milk 10 heads Experimental group 1 (G1) Milk powder + fat dietary supplement 1 10 heads Experimental group 2 (G2) Milk powder + fat dietary supplement 2 10 heads Experimental Group 3 (G3) Milk powder + fat dietary supplement 3 10 heads

[0256] The testing methods for the nutritional parameters mentioned in this article are as follows:

[0257] Serum biochemical index detection: Commercial kits (Leadman Biotech Limited, Beijing, China) and biochemical analyzers (Beckman CX4; Beckman Coulter, Germany) were used to analyze total protein (TP), albumin (ALB), urea nitrogen (BUN), creatinine (CRE), blood glucose (GLU), insulin (INS) (fasting insulin resistance index = fasting blood glucose × fasting insulin / 22.5, where the unit of fasting blood glucose is mmol / L and the unit of fasting insulin is μU / mL); immunoglobulins IgG, IgM; HDL-C, LDL-C, serum glutamate aminotransferase (ALT), serum aspartate aminotransferase (AST), serum total triglycerides (TG), total cholesterol (CHOL), D-lactic acid, and total bile acid (TBA) concentrations.

[0258] RT-PCR detection indicators: IL-1β, IL-6, TNF-α, TLR4, NF-κB, MUC-2 in duodenum, jejunum, and ileum. SREBP-1C, PPARγ, APOB, FAS, ACC, PPARα, ACOX, CPT-1α, HSL, etc. in longissimus dorsi muscle and back fat. The RT-QPCR method was referred to "B. Song, Dietary leucine supplementation improves intestinal health of mice through intestinal SIgA secretion, 2019".

[0259] Western blot analysis indicators: Ki-67, Occludin, Claudin, ZO-1, TLR4, NK-κB, mTOR, ULK1, TFEB, SREBP1, PPARγ, HIF1α, PINK, Parkin, p-mTOR in each intestinal segment; p-mTOR, Prdm16, Irisin in dorsal fat and perirenal fat; Slow MyHC, Fast MyHC, mTOR, AMPK, PGC-1α in dorsal muscle. The Western blot analysis method was referred to "B. Song, Dietary leucine supplementation improves intestinal health of mice through intestinal SIgA secretion, 2019".

[0260] ELISA analysis parameters: The ground tissues were tested according to the manufacturer's instructions (Jiancheng Bioengineering Institute, Nanjing, Jiangsu, China). Serum malondialdehyde (MDA), glutathione peroxidase (GSH-PX), superoxide dismutase (SOD); insulin, glucagon; stress hormones (cortisol and ACTH), D-xylose, IL-1β, IL-6, IL-10, TNF-α concentrations were measured using a commercial porcine ELISA kit (Cusabio Life Science, Inc., Wuhan, China). IL-1β, IL-6, IL-10, TNF-α concentrations in each intestinal segment. Spleen, jejunum, ileum: IgA, IgG, IgM. Aminopeptidase N, sucrase, and maltase activities in each intestinal segment, expression of 5-hydroxytryptamine, norepinephrine, substance P, and corticotropin-releasing factor. In plasma, spleen, and each intestinal segment: IgE and HIS.

[0261] Intestinal morphology: Referring to “JYYu, Development of intestinal injury and restoration of weaned piglets under chronic immune stress, 2022” and “J.Wang, Developmental changes in intercellular junctions and Kv channels in the intestine of piglets during the suckling and post-weaning periods, 2016”, fixed segments of the duodenum, jejunum, and ileum were subjected to morphological analysis using hematoxylin-eosin staining. Parameters such as villus height (VH) and crypt depth (CD) were determined under a microscope and measured using CaseViewer software. The ratio of VH to CD was calculated. Referring to “Y.Xiao, Ellagic acid alleviates oxidative stress by mediating Nrf2 signaling pathways and protects against paraquat-induced intestinal injury in piglets”, intestinal segments were cold-fixed with 2.5% glutaraldehyde for scanning and transmission electron microscopy analysis.

[0262] 7. Results

[0263] 7.1 Gut Health

[0264] (1) Intestinal mechanical barrier

[0265] Table 4 and Figure 1 The results show the effects of dietary treatment on the expression of tight junction proteins in the intestine of piglets. Figure 1 It can be seen that compared with the breast milk group (G0 group), the G1 group significantly reduced the protein expression abundance of tight junction-related proteins (Occludin, Claudin and ZO-1) in the duodenal, jejunal and ileal mucosa (P<0.05). Compared with the G1 group, the G3 group significantly increased the protein expression abundance of tight junction-related proteins (Occludin, Claudin and ZO-1) in the duodenal, jejunal and ileal mucosa (P<0.05). Compared with the G1 group, the protein expression abundance of tight junction-related proteins (Occludin, Claudin and ZO-1) in the duodenal, jejunal and ileal mucosa of the G2 group was also increased. These results indicate that compared with even-numbered fatty acids, dietary supplementation with odd-numbered fatty acids can improve the intestinal mechanical barrier of piglets by promoting the expression of tight junction proteins in intestinal epithelial cells; the higher the proportion of C15 in the composition of odd-numbered carbon chain fatty acids, the more it can improve the intestinal mechanical barrier of piglets by promoting the expression of tight junction proteins in intestinal epithelial cells (such as duodenal Occludin, duodenal Claudin, duodenal ZO-1, jejunal Occludin, jejunal Claudin, ileal Occludin, ileal Claudin, and ileal ZO-1).

[0266] Table 4

[0267] G0 G1 G2 G3 Duodenal Occlidin Protein 0.41 0.16 0.25 0.30 Duodenal Claudin Protein 0.32 0.12 0.26 0.31 Duodenal ZO-1 protein 0.34 0.07 0.13 0.21 Jejunal Occlidin Protein 0.26 0.08 0.21 0.22 Jejunal Claudin Protein 0.26 0.05 0.14 0.28 Jejunal ZO-1 protein 0.28 0.07 0.28 0.19 Ileal Occlidin Protein 0.21 0.07 0.14 0.18 Ileal Claudin 0.30 0.06 0.15 0.19 Ileal ZO-1 protein 0.23 0.06 0.15 0.24

[0268] Table 5 and Figure 2 The effects of dietary treatment on the levels of hormones released from the intestine of piglets are shown. Corticotropin-releasing hormone (CRF) is a releasing hormone involved in the stress response, mainly for the pituitary gland to synthesize adrenocorticotropic hormone. People tend to think that CRF is only related to the secretion of the central system, but the evidence in this application shows that the peripheral release of CRF plays a vital role in the permeability regulation of the gastrointestinal tract and is part of the connection between the gut-brain axis. Figure 2 It can be seen that compared with the breast milk group (G0 group), the G1 group significantly increased the CRF content in the ileum of piglets (P<0.05), suggesting that the mechanical barrier of the intestinal wall at the end of the small intestine may be weakened. However, compared with the G1 group, the CRF content in the ileum tissue of piglets in the G3 group decreased significantly (P<0.05), and the CRF content in the ileum tissue of piglets in the G2 group also decreased compared with the G1 group. These results show that compared with even-numbered carbon fatty acids, dietary supplementation with odd-numbered carbon fatty acids can also enhance or improve the mechanical barrier function of the piglet intestine by reducing the content of CRF in intestinal tissue.

[0269] Table 5

[0270] G0 G1 G2 G3 Ileal corticotropin-releasing factor (CRF) 374.17 430.98 336.85 403.84

[0271] (2) Intestinal immune homeostasis

[0272] Table 6-1 and Figure 3 The effect of dietary treatment on immunoglobulin in piglet jejunum is shown. Immunoglobulin is a class of proteins with antibody activity in the human body. Immunoglobulin is an important component for the body to resist disease. It has antibacterial and antiviral effects and enhances the phagocytic function of cells. It can kill or dissolve pathogenic microorganisms with the cooperation of complement. IgG, IgM, and IgA are usually tested. IgG accounts for 75% of total immunoglobulins and is the most persistent and important antibody in the primary immune response. IgA is the first line of defense against pathogen invasion. IgM plays an important role in early defense. From Figure 3 It can be seen that the jejunal IgG, IgA and IgM in the G3 group were significantly increased compared with the G1 group (P<0.05); the jejunal IgG protein and IgM protein in the G2 group were also increased compared with the G1 group. These results indicate that compared with even-numbered fatty acids, dietary supplementation with odd-numbered fatty acids can maintain jejunal immune homeostasis by increasing the content of jejunal immunoglobulins.

[0273] Table 6-1

[0274] G0 G1 G2 G3 Jejunal immunoglobulin G (IgG) 409.07 383.43 465.45 426.07 Jejunal immunoglobulin A (IgA) 42.96 43.61 44.71 46.90 Jejunal immunoglobulin M (IgM) 42.69 40.79 47.35 46.09

[0275] Table 6-2 and Figure 4 The effects of dietary treatment on ileal immunoglobulins in piglets were shown. Figure 4 It can be seen that compared with the G1 group, the IgA in the ileum of the G3 group was significantly increased (P<0.05), while there was no significant change in IgG and IgM. IgA is the first line of defense against pathogen invasion, indicating that compared with even-numbered fatty acids, dietary supplementation with odd-numbered fatty acids can enhance the ability of the jejunum to resist pathogen invasion and improve jejunal immunity by increasing the content of immunoglobulin IgA in the ileum.

[0276] Table 6-2

[0277] G0 G1 G2 G3 Ileal immunoglobulin G (IgG) 440.25 422.98 424.97 409.30 Ileal immunoglobulin A (IgA) 40.63 43.11 36.09 46.13 Ileal immunoglobulin M (IgM) 46.72 46.93 40.37 47.56

[0278] Table 7 and Figure 5 The results show the effect of dietary treatment on the TLR4 / NF-κB signaling pathway in the intestine of piglets. Inflammatory response is an important immune defense mechanism of the body. Normal inflammatory response is a manifestation of the body's immunity and is beneficial to the body. TLR4 / NF-κB is the body's inflammatory response signaling pathway. Figure 5It can be seen that compared with the breast milk group (G0 group), the protein expression abundance of inflammatory response-related genes (TLR4 and NF-κB) in the duodenum, jejunum and ileum of piglets in the G1 group was significantly decreased (P<0.05), indicating that the change in diet led to changes in intestinal immune homeostasis. Compared with the G1 group, the G3 group significantly upregulated the protein expression abundance of TLR4 and NF-κB in the duodenum, jejunum and ileum (P<0.05); compared with the G1 group, the protein expression abundance of TLR4 and NF-κB in the duodenum, jejunum and ileum of the G2 group was also upregulated. These results suggest that compared with even-numbered carbon fatty acids, dietary supplementation of odd-numbered carbon fatty acids can maintain intestinal immune homeostasis by regulating the expression of the TLR4 / NK-κB signaling pathway; in the composition of odd-numbered carbon chain fatty acids, the higher the proportion of C15, the more it can maintain intestinal immune homeostasis by regulating the expression of the TLR4 / NK-κB signaling pathway.

[0279] Table 7

[0280] G0 G1 G2 G3 Duodenal Toll-like receptor-4 (TLR-4) 0.29 0.08 0.17 0.24 NF-kB 0.46 0.13 0.26 0.29 Jejunal Toll-like receptor-4 (TLR-4) 0.39 0.16 0.35 0.26 NF-kB 0.33 0.03 0.11 0.15 Ileal Toll-like receptor-4 (TLR-4) 0.27 0.04 0.16 0.23 NF-kB 0.32 0.05 0.14 0.23

[0281] Table 8 and Figure 6 The effects of dietary treatments on inflammatory cytokines (TNF-α, IL-1β, IL-6 and IL-10) in the ileum of piglets are shown. Inflammation induces the release of chemicals from damaged cells, and these released chemicals are generally referred to as inflammatory cytokines. Cytokines act as messenger molecules between cells, interacting with cells of the immune system, regulating the body's response to disease and infection, and mediating the activity of normal cells in the body. Figure 6 It can be seen that compared with the breast milk group (G0 group), the ileum inflammatory cytokines in the G1 group changed (P<0.05), indicating that dietary changes lead to changes in ileum immune homeostasis. Compared with G1, the G3 and G2 groups were able to adjust the inflammatory cytokines closer to the breast milk group, indicating that compared with even-numbered fatty acids, dietary supplementation with odd-numbered fatty acids can maintain ileum immune homeostasis by regulating inflammatory cytokines.

[0282] Table 8

[0283] G0 G1 G2 G3 Ileal tumor necrosis factor (TNF-a) 456.00 401.73 420.40 441.79 Ileal interleukin-1β (IL-1β) 46.41 48.58 44.42 40.74 Ileal interleukin-6 (IL-6) 1258.04 1065.78 1104.21 1266.52 Ileal interleukin-10 (IL-10) 166.54 211.31 173.33 198.35

[0284] Table 9 and Figure 7 The results show the effect of dietary treatment on the level of mucin 2 in the ileum of piglets. Mucin 2 (MUC-2) is one of the main components of the intestinal mucus layer, secreted by goblet cells, and can form a gelatinous matrix that accommodates antibacterial molecules, thereby effectively preventing the invasion of bacteria, viruses, etc. into the intestinal mucosa. Figure 7As shown in the figure, compared with the breast milk group (G0 group), the expression of ileal mucin 2 in the G1 group was significantly decreased, indicating that the immune function of the ileal mucosa was reduced (P<0.05). However, the expression of ileal mucin 2 in the G2 and G3 groups was restored to the level of the breast milk group, indicating that compared with the even-numbered fatty acids, dietary supplementation of odd-numbered fatty acids can also maintain the level of mucin in the mucosa and jointly maintain the immune homeostasis of the ileum.

[0285] Table 9

[0286] G0 G1 G2 G3 Ileal mucin 2 (MUC2) 1.62 0.95 1.57 1.52

[0287] Table 10 and Fig.37 The results show the effect of dietary treatment on the relative expression of hypoxia-inducible factor HIF-1α in the intestine of piglets. The intestinal environment is usually in a hypoxic state. As the main regulator of cellular response to hypoxia, HIF-1α plays an important role in intestinal homeostasis and host-microbe interaction. For example, some of its target genes can participate in intestinal barrier function. Fig.37 It can be seen that the expression of HIF-1α in the G3 group was significantly higher than that in the G1 group, indicating that compared with even-numbered fatty acids, dietary supplementation with odd-numbered fatty acids can increase the expression of HIF-1α in the intestine, thereby promoting the survival of intestinal cells in the intestinal hypoxic environment and benefiting intestinal homeostasis.

[0288] Table 10

[0289] G0 G1 G2 G3 Hypoxia-inducible factor 1-alpha (HIF-1α) in duodenum 0.28 0.04 0.23 0.19 Hypoxia-inducible factor 1-alpha (HIF-1α) 0.30 0.09 0.15 0.25 Ileal hypoxia-inducible factor 1-alpha (HIF-1α) 0.40 0.05 0.14 0.26

[0290] (3) Intestinal development

[0291] Figures 38 to 42 The results of intestinal development-related tests are shown. Scanning electron microscopy ( Fig.38 ) showed that the intestinal villi of the piglets in groups G2 and G3 were longer, thicker and denser than those in group G1, especially the intestinal villi of group G3 were comparable to those of group G0. Fig.39 As shown in the figure, the duodenum, jejunum, and ileum of the piglets in groups G2 and G3 showed better intestinal morphology than those in group G1, and were closer to the intestinal morphology of the piglets in group G0 fed with breast milk. The functional unit of the small intestine is the villi. Longer villi have more absorptive cells, and deeper crypts lead to less contact between intestinal cells and nutrients. The height of the small intestine villi (VH) and the ratio of the height of the villi to the depth of the crypts (CD) (VH:CD) are often used as indicators to evaluate the quality of the small intestine development. Figures 40-42 The results showed that the intestinal VH and VH:CD of the piglets in the G1 group were significantly lower than those in the G0 group (all P < 0.05), and the CD was deeper (all P < 0.05), indicating that milk powder feeding would have an adverse effect on the intestinal tract of piglets. Fig.40As shown in Table 11-1, in the duodenum, the VH:CD ratios of the G2 and G3 groups were significantly higher than those of the G1 group (P<0.05), and the VH, CD, and VH:CD ratios of the G2 and G3 groups were not significantly different from those of the G0 group. Fig.41 As shown in Table 11-2, in the jejunum, the VH:CD of the G2 group was significantly higher than that of the G1 group (P<0.05), and the CD was significantly lower than that of the G1 group (P<0.05); the VH and VH:CD of the G3 group were significantly higher than those of the G1 group (P<0.05), and the CD was significantly lower than that of the G1 group (P<0.05), and there was no significant difference between the above indicators and the G0 group. Fig.42 As shown in Table 11-3, in the ileum, the VH:CD of the G2 and G3 groups was significantly higher than that of the G1 group (P<0.05), and the CD was significantly lower than that of the G1 group (P<0.05), and the above indicators were close to those of the G0 group. In summary, the above results prove that odd-numbered carbon fatty acids are beneficial to improving intestinal morphology, increasing VH and VH:CD, reducing CD, and are beneficial to intestinal development, and enable the intestinal development of milk powder-fed animals to reach a level comparable to that of the breast milk group.

[0292] Table 11-1

[0293] G0 G1 G2 G3 Duodenal villus height 332.25 308.14 324.97 329.91 Depth of duodenal recess 289.28 330.00 305.28 292.43 Ratio of duodenal villus height to crypt depth 1.15 0.94 1.06 1.13

[0294] Table 11-2

[0295] G0 G1 G2 G3 Jejunal villus height 348.35 326.15 327.21 341.69 Jejunal crypt depth 141.41 208.38 175.09 155.70 Ratio of jejunal villus height to crypt depth 2.50 1.57 1.89 2.20

[0296] Table 11-3

[0297] G0 G1 G2 G3 Ileal villus height 296.40 283.48 287.37 295.29 Ileal crypt depth 96.12 172.30 134.43 115.12 Ratio of ileal villus height to crypt depth 3.15 1.65 2.14 2.57

[0298] Table 12 and Figure 8 The results show the effect of dietary treatment on the proliferation of intestinal epithelial cells in piglets. Ki67 is a proliferating cell-related antigen, and its function is closely related to mitosis. It is indispensable in cell proliferation. The higher the expression level of Ki67, the more active the cell proliferation. Figure 8 It can be seen that the protein expression abundance of Ki67 in the intestinal epithelial cells of the G3 group was significantly higher than that of the G1 group (P<0.05), and the protein expression abundance of Ki67 in the intestinal epithelial cells of the G2 group was significantly higher than that of the G1 group. These results indicate that compared with even-numbered carbon fatty acids, dietary supplementation with odd-numbered carbon fatty acids can improve the intestinal mechanical barrier and promote intestinal development by promoting intestinal epithelial cell proliferation; the higher the proportion of C15 in the composition of odd-numbered carbon chain fatty acids, the more it can improve the intestinal mechanical barrier and promote intestinal development by promoting intestinal epithelial cell proliferation.

[0299] Table 12

[0300] G0 G1 G2 G3 Duodenal nuclear protein Ki-67 (Ki-67) 0.33 0.11 0.21 0.21 Jejunal nuclear protein Ki-67 (Ki-67) 0.36 0.05 0.28 0.30 Ileal nuclear protein Ki-67 (Ki-67) 0.20 0.04 0.11 0.15

[0301] Table 13 and Fig. 9 The results show the effect of dietary treatment on the level of mTOR protein in the small intestine of piglets. mTOR (mammalian target of rapamycin) protein is a kinase that is regulated by growth factors and environmental nutrient levels. It can interact with a variety of proteins, activate or inhibit downstream signaling pathways, thereby promoting the occurrence of ribosomes, the synthesis of proteins, lipids and nucleic acids, inhibiting cell autophagy, and promoting cell growth and proliferation. It plays an important role in regulating cell processes and tissue development. Compared with the breast milk group (G0 group), the expression level of phosphorylated (activated) mTOR protein in the G1 group was significantly reduced (P<0.05), indicating that the normal growth activity of cells was inhibited. The G3 group was able to increase the expression of activated mTOR protein in small intestinal cells to the level of the breast milk group or similar levels; in addition, the expression of activated mTOR protein in small intestinal cells in the G2 group was also higher than that in the G1 group. These results indicate that dietary supplementation with odd-carbon fatty acids can activate the mTOR signaling pathway and contribute to cell growth and tissue development; the higher the proportion of C15 in the composition of odd-carbon chain fatty acids, the more it can activate the mTOR signaling pathway and contribute to cell growth and tissue development.

[0302] Table 13

[0303] G0 G1 G2 G3 Phosphorylated mammalian target of rapamycin (p-mTOR) in the duodenum 0.38 0.12 0.21 0.30 Phosphorylated mammalian target of rapamycin (p-mTOR) in jejunum 0.32 0.03 0.19 0.27 Phosphorylated mammalian target of rapamycin (p-mTOR) in the ileum 0.25 0.06 0.13 0.16

[0304] Table 14 and Fig.10 The effects of treatment on the level of p70S6K in the small intestine of piglets are shown. p70S6K (p70 ribosomal S6 kinase) is a type of protein kinase involved in signal transduction, which can be activated by mTOR protein and regulate cell proliferation and tissue development by regulating protein synthesis and ribosome biogenesis. Similar to the expression status of mTOR protein, the level of phosphorylated (activated) S6 kinase in the G1 group was significantly reduced compared with the breast milk group (G0 group) (P<0.05), indicating that the normal growth of cells was inhibited. The G3 group was able to increase the level of activated S6 kinase in small intestinal cells to the level of the breast milk group or similar levels, and the level of activated S6 kinase in the small intestinal cells of the G2 group was also significantly higher than that of the G1 group, indicating that dietary supplementation with odd-numbered carbon fatty acids can rescue cell proliferation and protein metabolism in small intestinal tissues and promote tissue development. This regulation may be mediated by the mTOR signaling pathway; the higher the proportion of C15 in the composition of odd-numbered carbon chain fatty acids, the more it can rescue cell proliferation and protein metabolism in small intestinal tissues and promote tissue development.

[0305] Table 14

[0306] G0 G1 G2 G3 Phosphorylated p70S6 kinase in duodenum (p-p70S6K) 0.45 0.06 0.28 0.37 Phosphorylated p70S6 kinase (p-p70S6K) in jejunum 0.39 0.07 0.15 0.22 Ileal phosphorylated p70S6 kinase (p-p70S6K) 0.35 0.07 0.19 0.26

[0307] Table 15 and Fig.11The results show the effect of dietary treatment on the digestive enzyme levels in the small intestine of piglets. Maltase, aminopeptidase (APN) and invertase are digestive enzymes on the brush border of the small intestine, which can reflect the digestive and absorptive function of the intestine and are important indicators of the physiological function and developmental maturity of the intestine. Fig.11 It can be seen that compared with the breast milk group (G0 group), the digestive enzyme level of the G1 group was significantly different (P<0.05), indicating that the change in diet led to changes in the digestive capacity of the small intestine. The G3 group was able to increase the level of small intestinal digestive enzymes, reaching or even exceeding the level of the breast milk group, indicating that dietary supplementation of odd-numbered fatty acids can help fully absorb nutrients by increasing the level of small intestinal digestive enzymes.

[0308] Table 15

[0309] G0 G1 G2 G3 Duodenal Maltase 164.88 176.14 178.74 187.66 Ileal aminopeptidase N (AP-N) 400.69 322.05 384.06 384.75 Ileal invertase 275.93 279.51 273.79 296.57

[0310] Table 16 and Fig.12 The effect of dietary treatment on the levels of neurotransmitters and neuropeptides in the small intestine of piglets is shown. 5-hydroxytryptamine (5-HT) is a type of monoamine neurotransmitter, which is mainly synthesized in the chromaffin cells of the small intestine of animals, and is also found in small amounts in platelets and the central nervous system, playing different functions in different tissues. About 90% of the 5-hydroxytryptamine in the animal body is present in gastrointestinal cells and myenteric plexus, and is involved in the regulation of intestinal peristalsis. Substance P (SP) is also widely distributed in the gastrointestinal tract, mainly promoting the contraction of gastrointestinal smooth muscle, inhibiting gastric acid and bile secretion, and regulating local gastrointestinal blood flow. As shown in the figure above, compared with the breast milk group (G0 group), the content of neurotransmitters and neuropeptides in the small intestine of the G1 group was similar or slightly reduced. However, the G3 group could significantly increase the level of 5-hydroxytryptamine in the duodenum, jejunum and ileum and the content of substance P in the ileum, restoring them to the level of or above that of the breast milk group. The G2 group could significantly increase the level of 5-hydroxytryptamine in the duodenum, suggesting that dietary supplementation with odd-numbered fatty acids can enhance the function of the small intestine by increasing the level of gut-brain peptides related to the gut-brain axis.

[0311] Table 16

[0312] G0 G1 G2 G3 Duodenal serotonin (5-HT) 46.45 45.44 55.01 48.54 Jejunal serotonin (5-HT) 47.26 47.74 44.63 50.67 Ileal serotonin (5-HT) 50.57 48.28 44.90 52.44 Ileal neuropeptide substance P (SP) 216.94 225.28 222.05 238.48

[0313] (4) Intestinal energy metabolism

[0314] Table 17 and Fig.13 The results show the effect of dietary treatment on the level of mitophagy in the small intestine of piglets. Mitophagy is a process of programmed degradation of mitochondria in cells, which mostly occurs in damaged or defective mitochondria and is used to prevent the accumulation of dysfunctional mitochondria and thus cause cell abnormalities. Fig.13As shown in the figure, compared with the breast milk group (G0 group), the expression levels of key mitophagy proteins (ULK1, TFEB and Parkin) in the G1 group were significantly increased (P<0.05), indicating excessive accumulation of abnormal mitochondria in the cells. The G2 and G3 groups were able to downregulate the expression levels of intracellular mitophagy-related proteins to a level similar to that of the breast milk group, indicating that compared with even-carbon fatty acids, dietary supplementation of odd-carbon fatty acids can alleviate mitochondrial dysfunction and help maintain the energy homeostasis of intestinal cells; in the composition of odd-carbon chain fatty acids, the higher the proportion of C15, the more it can alleviate mitochondrial dysfunction and help maintain the energy homeostasis of intestinal cells.

[0315] Table 17

[0316] G0 G1 G2 G3 Duodenal Unc-51-like autophagy-activating kinase (ULK1) 0.14 0.30 0.20 0.19 Duodenal transcription factor EB (TFEB) 0.10 0.36 0.28 0.24 Duodenal ubiquitin ligase (Parkin) 0.13 0.38 0.21 0.19 Jejunal Unc-51-like autophagy-activating kinase (ULK1) 0.09 0.40 0.31 0.18 Transcription factor EB (TFEB) 0.10 0.30 0.22 0.18 Jejunal ubiquitin ligase (Parkin) 0.10 0.32 0.24 0.13 Ileal Unc-51-like autophagy-activating kinase (ULK1) 0.09 0.42 0.21 0.17 Ileal transcription factor EB (TFEB) 0.07 0.33 0.17 0.10

[0317] Table 18 and Fig.14 The results show the effect of dietary treatment on the lipid metabolism level in the small intestine of piglets. Lipids are important functional substances in the body and cells and are the main form of energy storage. The activity of lipid metabolism can reflect the overall energy state of the tissue. PPARγ and SREBP-1 are transcription factors related to lipid metabolism in cells and are closely related to lipid uptake and synthesis. As shown in the above figure, compared with the breast milk group (G0 group), the content of PPARγ and SREBP-1 in the duodenum and jejunum of the G1 group was significantly reduced (P<0.05), indicating that lipid synthesis was inhibited and the cellular energy state was abnormal. The G2 and G3 groups were able to upregulate the levels of lipid synthesis-related transcription factors and reached or approached the level of the breast milk group to a certain extent, indicating that dietary supplementation of odd-carbon fatty acids can improve the absorption and anabolism of lipids in the small intestine of piglets, which is beneficial to maintaining the energy homeostasis of intestinal cells; in the composition of odd-carbon chain fatty acids, the higher the proportion of C15, the better the absorption and anabolism of lipids in the small intestine of piglets, which is beneficial to maintaining the energy homeostasis of intestinal cells.

[0318] Table 18

[0319] G0 G1 G2 G3 Duodenal peroxisome proliferator-activated receptor gamma (PPARγ) 0.31 0.04 0.17 0.22 SREBP-1 0.45 0.14 0.35 0.34 Jejunal peroxisome proliferator-activated receptor gamma (PPARγ) 0.36 0.05 0.20 0.24 Jejunal sterol regulatory element binding transcription factor 1 (SREBP-1) 0.31 0.07 0.30 0.29

[0320] (5) Development and metabolism of muscle tissue

[0321] Muscle tissue is composed of muscle fibers (cells), and muscle cells can be divided into type I fibers (MYHC I) and type II fibers (MYHC II) according to their appearance and function. Type I fibers are also called red muscle fibers, slow muscle fibers or slow oxidative fibers. These muscle fibers have slow contraction speed, low strength, good oxygen utilization and good endurance. Type II fibers are called white muscle fibers, fast muscle fibers or fast glycolysis fibers. They mainly provide short-term energy through glycolysis and have poor endurance, but they have a strong effect on improving the explosive power and speed of exercise, and are also the main factors determining muscle strength and speed. At the same time, the cross-sectional area of ​​fast muscle fibers is thicker, and muscle tissue rich in fast muscle fibers is easy to develop and grow strong. In animal nutrition, the number of fast muscle fibers is significantly correlated with the meat production of animals, and is also an indicator of concern in animal production. mTOR also plays an important role in muscle tissue, which can control the anabolism and catabolism signals of skeletal muscle, thereby achieving the regulation of muscle enlargement and muscle atrophy. AMPK (AMP-activated protein kinase) is an energy-sensing enzyme that is activated when cellular energy levels are low (elevated ADP and AMP levels). PCG1-α is the main regulator that induces the conversion of type II muscle fibers to type I.

[0322] As shown in Table 19 and Fig.15 As shown in the results, compared with the breast milk group (G0 group), the content of type I and type II muscle fibers and the expression of mTOR protein in the back muscle tissue of the G1 group were significantly reduced (P<0.05), while the content of AMPK and PGC1-α increased significantly (P<0.05). This means that the muscle tissue of the piglets in the G1 group is in a state of energy deficiency, cell proliferation slows down, and the transformation of type II muscle fibers to type I muscle fibers continues to occur, resulting in the loss of muscle mass in the body. The G3 group was able to significantly increase the content of type I and type II muscle fibers and the expression of mTOR protein in muscle tissue (P<0.05), while reducing the relative content of AMPK and PGC1-α (P<0.05); the G2 group was also able to increase the content of type I and type II muscle fibers and the expression of mTOR protein in muscle tissue, while reducing the relative content of AMPK and PGC1-α. This shows that dietary supplementation with odd-numbered fatty acids can improve the energy status of muscle tissue, promote cell proliferation and tissue development, increase muscle fiber content, inhibit the transformation of type II muscle fibers to type I muscle fibers, increase muscle mass, and ultimately promote the overall development of muscle tissue; the higher the proportion of C15 in the odd-numbered carbon chain fatty acid composition, the more it can improve the energy status of muscle tissue, promote cell proliferation and tissue development, increase muscle fiber content, inhibit the transformation of type II muscle fibers to type I muscle fibers, increase muscle mass, and ultimately promote the overall development of muscle tissue.

[0323] Table 19

[0324] G0 G1 G2 G3 Dorsal muscle myosin heavy chain 1 (MYHC1) 0.37 0.05 0.17 0.20 Dorsal muscle myosin heavy chain 2a (MYHC2a) 0.37 0.07 0.19 0.26 Dorsal muscle myosin heavy chain 2b (MYHC2b) 0.32 0.04 0.13 0.17 Dorsal muscle myosin heavy chain 2x (MYHC2x) 0.34 0.05 0.15 0.22 Dorsal muscle mammalian target of rapamycin (mTOR) 0.32 0.04 0.12 0.19 Phosphorylated AMP-activated protein kinase (p-AMPK) in dorsal muscle 0.05 0.38 0.24 0.18 Dorsal muscle peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) 0.06 0.33 0.22 0.20

[0325] Muscle is the main target organ for energy metabolism and glucose and lipid metabolism in the body, and has active lipid metabolism, especially during exercise. SREBP-1 is a transcription factor related to lipid metabolism in cells and is closely related to lipid uptake and synthesis. Fig.16 As shown in the figure, compared with the breast milk group (G0 group), the SREBP-1 content in the G1 group decreased to a certain extent, but it was not significant. However, the G2 and G3 groups were able to significantly upregulate the expression of SREBP-1 in muscle tissue, indicating that there is more active lipid anabolism in muscle tissue. This shows that dietary supplementation of odd-carbon fatty acids can increase the uptake and utilization of lipids by muscle tissue, improve energy status, and promote the development of muscle tissue, which can also correspond to the above-mentioned increase in muscle cell proliferation and muscle mass.

[0326] Table 20

[0327] G0 G1 G2 G3 SREBP-1C 1.08 0.82 2.73 1.94

[0328] (6) Development and metabolism of adipose tissue

[0329] Similar to the other tissues mentioned above, mTOR protein is an important part of lipid production and maintenance in adipose tissue, as well as adipose tissue development. Transcription factors containing the 16PR domain (Prdm16) and irisin can act on white fat cells to induce their conversion into brown fat cells. Although the content of brown adipose tissue in adults is small, its heat production efficiency is extremely high. A small piece of brown fat can burn a lot of calories. Activated brown adipose tissue generates heat by rapidly consuming glucose and fat, which is very important for fighting obesity. Therefore, Prdm16 and Irisin are the molecular switches for the browning of white fat and are related to lipolysis. In the early stages of animal development, a certain amount of fat storage plays an important role in the body's overall energy metabolism and homeostasis. From Tables 21 and Fig.17 As shown in the figure, compared with the breast milk group (G0 group), the content of activated mTOR protein in the back fat and perirenal fat of piglets in the G1 group was significantly reduced (P<0.05), and Prdm16 and Irisin were significantly increased (P<0.05), indicating that lipid synthesis and the development of adipose tissue were blocked, and the browning process of white fat was aggravated, and lipolysis was obvious. The G2 and G3 groups were able to significantly upregulate the expression of activated mTOR and reduce the expression of Prdm16 and Irisin, which means that dietary supplementation with odd-numbered carbon fatty acids can inhibit lipolysis and increase lipid synthesis for the development of adipose tissue; in the composition of odd-numbered carbon chain fatty acids, the higher the proportion of C15, the more it can inhibit lipolysis and increase lipid synthesis for the development of adipose tissue.

[0330] Table 21

[0331] G0 G1 G2 G3 Mammalian target of rapamycin (mTOR) 0.44 0.12 0.34 0.34 Dorsal fat transcription factor containing 16PR domain (Prdm16) 0.06 0.38 0.27 0.15 Irisin 0.09 0.45 0.37 0.24 Perinephric lipid mammalian target of rapamycin (mTOR) 0.46 0.12 0.28 0.33 Perinephric lipid transcription factor containing 16PR domain (Prdm16) 0.10 0.43 0.31 0.25

[0332] Similarly, SREBP-1 is a transcription factor related to lipid metabolism in cells and is closely related to lipid uptake and synthesis. APOB (apolipoprotein) is the main component of lipoprotein and is responsible for the transport of lipids in various systems. Fig.18 As shown in the figure, compared with the breast milk group (G0 group), the SERBP-1 level of piglets in the G1 group was similar, but APOB was significantly reduced (P<0.05), suggesting that lipid transport may be blocked. The G3 group significantly upregulated the level of SERBP-1 in the adipose tissue of piglets and restored the APOB level to the level of the breast milk group (P<0.05). This means that dietary supplementation with odd-numbered carbon fatty acids can increase lipid synthesis in adipose tissue and enhance the body's transport of lipids, which helps maintain the energy balance of adipose tissue and the body.

[0333] Table 22

[0334] G0 G1 G2 G3 Sterol regulatory element binding transcription factor 1 (SREBP-1C) 0.88 1.33 1.64 2.76 Apolipoprotein B (APOB) 1.12 0.40 1.86 0.95

[0335] (7) Body redox state

[0336] Glutathione peroxidase (GSH-PX) is a class of enzymes with peroxidase activity that play a role in detoxification in organisms. Its main biological function is to reduce lipid peroxides to corresponding alcohols and free hydrogen peroxide to water, which has antioxidant properties. As shown in Table 23 and Fig.19 As shown in the figure, compared with the breast milk group (G0 group), the GSH-PX content of piglets in the G1 group was significantly reduced, which means that their antioxidant capacity was weakened and the cell structure was easily damaged by peroxides. The G2 and G3 groups significantly increased the GSH-PX content in the serum of piglets and restored it to a level close to that of the breast milk group. This means that dietary supplementation with odd-numbered carbon fatty acids can improve the body's overall antioxidant capacity and help maintain the overall redox balance.

[0337] Table 23

[0338] G0 G1 G2 G3 Serum glutathione peroxidase (GSH-Px) 194.95 160.54 177.90 186.16

[0339] (8) Allergic reactions of the body and intestines

[0340] The stronger the allergic reaction, the more IgE and HIS are released. Fig. 20As shown in the results, G3 significantly reduced blood HIS (P<0.05), jejunal IgE (P<0.05), ileal IgE (P<0.05) and HIS (P<0.05) compared with G1, and jejunal IgE and ileal IgE in G2 group also decreased compared with G1 group. This indicates that compared with even-numbered fatty acids, dietary supplementation of odd-numbered fatty acids is beneficial to reducing allergic reactions of the body and the jejunum and ileum.

[0341] Table 24

[0342] G0 G1 G2 G3 Serum immunoglobulin E (IgE) 34.87 31.54 38.07 31.75 Serum histamine (HIS) 14.25 15.50 15.79 13.85 Jejunal immunoglobulin E (IgE) 32.66 35.49 31.65 32.64 Jejunal histamine (HIS) 13.22 13.04 12.97 13.19 Ileal immunoglobulin E (IgE) 34.36 34.60 33.14 31.14 Ileal histamine (HIS) 11.86 13.17 13.02 12.18

[0343] (10) Nutritional effects

[0344] 4.1 Growth performance

[0345] As shown in Table 25 and Fig.21 As shown, dietary supplementation with odd-numbered fatty acids had no significant effect on average daily gain, average daily feed intake and feed weight of piglets.

[0346] Table 25

[0347] G0 G1 G2 G3 Average daily gain (ADG) of piglets during the trial period 263.75 313.92 301.75 331.75 Average daily feed intake (ADFI) of piglets during the trial period 291.06 270.63 299.81 Feed-to-weight ratio (FCR) of piglets during the trial period 0.93 0.90 0.91

[0348] As shown in Table 26 and Fig. 22 As shown, dietary supplementation with odd-numbered fatty acids did not affect the weights of the liver, cerebrum, cerebellum, and brainstem in piglets.

[0349] Table 26

[0350] G0 G1 G2 G3 Liver to body weight ratio (LwR) 1.94 2.97 2.79 2.88 Brain to Body Mass Ratio (BwR) 0.53 0.51 0.50 0.48 Cerebellum to body weight ratio 0.08 0.07 0.07 0.06 Brain stem to body weight ratio 0.04 0.04 0.03 0.03

[0351] During the trial period, the piglets' feces were observed every day, and it was found that the piglets had no obvious diarrhea and their growth was good throughout the whole process, indicating that dietary supplementation of odd-numbered fatty acids would not cause diarrhea in piglets.

[0352] The non-specific reaction of individuals caused by various stress stimuli (stressors) is a stress reaction. Long-term stress reactions can cause symptoms. When the body has an emergency response, the levels of cortisol and adrenocorticotropic hormone (ACTH) in the blood will increase. As shown in Table 27 and Fig.23 As shown, there was no significant difference in blood stress hormones (cortisol and adrenocorticotropic hormone (ACTH)) between the G1 and G3 groups (P>0.05), and there was no significant difference between the G1 and G3 groups, indicating that dietary supplementation with odd-numbered fatty acids did not cause stress response in lactating piglets.

[0353] Table 27

[0354] G0 G1 G2 G3 Serum cortisol 191.00 190.36 204.90 189.52 Serum adrenocorticotropic hormone (ACTH) 135.35 140.95 137.31 134.95

[0355] Abnormal lipid metabolism may lead to increased triglycerides (TG), cholesterol (CHOL), and low-density lipoprotein (LDL-C) in the blood, decreased high-density lipoprotein (HDL-C), and liver damage (if the liver is damaged, the aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in the blood will increase). As shown in Table 28 and Fig.24 As shown, there was no significant difference in TG, CHOL, HDL-C and LDL-C in the blood of piglets in the G1 group, G2 group and G3 group, and there was no significant difference in AST and ALT. This shows that compared with even-numbered carbon fatty acids, dietary supplementation of odd-numbered carbon fatty acids did not lead to abnormal lipid metabolism in the body.

[0356] Table 28

[0357] G0 G1 G2 G3 Serum high-density lipoprotein cholesterol (HDL-C) 1.29 0.86 0.98 0.97 Serum low-density lipoprotein cholesterol (LDL-C) 1.45 1.00 1.08 1.05 Serum alanine aminotransferase (ALT) 43.50 36.95 34.91 37.56 Serum aspartate aminotransferase (AST) 151.68 121.38 113.00 92.14 Serum total triglyceride (TG) 1.46 0.54 0.54 0.44 Serum total cholesterol (CHOL) 4.00 2.81 2.67 2.42

[0358] Table 29 and Fig.25 The results show the effects of dietary treatment on blood protein metabolism related parameters in piglets. Fig.25 It can be seen that dietary supplementation with odd-numbered fatty acids will not affect blood protein metabolism.

[0359] Table 29

[0360] G0 G1 G2 G3 Serum total protein (TP) 45.24 37.23 36.69 40.03 Serum albumin (ALB) 35.08 25.93 25.14 28.83 Serum urea nitrogen (BUN) 3.08 1.04 0.99 1.00 Serum creatinine (CREA) 74.00 50.13 44.88 49.25

[0361] TNF-α is a cytokine involved in systemic inflammation, mainly secreted by macrophages, which can cause acute phase reactions, promote fever, and cause cell apoptosis. The content of TNF-α in serum can be used as an indicator factor to reflect the overall inflammatory status of the body to a certain extent. Table 30 and Fig.26 The effects of dietary treatment on key indicators of serum inflammation in piglets were shown. Fig.26 It can be seen that compared with the G0 and G1 groups, dietary supplementation with odd-numbered fatty acids did not impose an additional burden on the overall inflammatory status of piglets.

[0362] Table 30

[0363] G0 G1 G2 G3 Serum tumor necrosis factor (TNF-a) 415.13 470.40 458.85 476.79

[0364] Table 31 and Fig. 27 The effect of dietary treatment on immunoglobulins in piglet blood and spleen is shown. As can be seen from the figure, there is no significant difference in IgG and IgM in the blood of piglets in groups G2 and G3 compared with group G1, and there is no difference in the level of IgA in the liver, indicating that compared with even-numbered fatty acids, dietary supplementation of odd-numbered fatty acids did not lead to significant changes in the body's humoral immunity.

[0365] Table 31

[0366] G0 G1 G2 G3 Serum immunoglobulin G (IgG) 1.67 1.26 1.45 1.44 Serum immunoglobulin M (IgM) 0.34 0.23 0.27 0.25 Spleen immunoglobulin A (IgA) 41.24 40.83 46.44 42.04

[0367] D-lactic acid (LACT) is the metabolic end product of gastrointestinal bacteria. Mammals do not have an enzyme system that can quickly metabolize and decompose it, so an increase in the level of D-lactic acid in the blood can reflect changes in intestinal permeability. Fig.28 The effects of dietary treatment on D-lactic acid in piglet blood are shown in Table 32 and Fig.28 It can be seen that there is no significant difference in D-lactic acid in the serum of piglets in the G2 and G3 groups compared with G1, indicating that compared with even-numbered carbon fatty acids, dietary supplementation of odd-numbered carbon fatty acids did not lead to significant changes in the body's intestinal permeability.

[0368] Table 32

[0369] G0 G1 G2 G3 Serum D-lactic acid (D-LACT) 7.26 3.76 4.99 4.60

[0370] Example 2

[0371] 1. Basic process of the experiment

[0372] In this experiment, pregnant rats were fed with normal diet and low-protein diet (abnormal diet) containing OCFA oil and OCFA oil (Hard ST and high oleic sunflower oil were used to eliminate the influence of DHA, SFA and UFA ratio, n-3 and n-6 ​​unsaturated fatty acid ratio in OCFA algae oil), and gavage was performed on the 7.5th day of pregnancy. The rats were fasted for 6 hours from the 18.5th day of pregnancy, anesthetized with ether, and killed for sampling.

[0373] Unless otherwise stated, the various detection methods of this example are the same as those of Example 1.

[0374] 2. Oil Preparation

[0375] Oil 1: DHA algae oil (obtained by refining crude oil purchased from Qingdao Keyuan, the refining method refers to Huang Huaixin's "Optimization of Microalgae DHA Refining Process", crude oil batch MKD120056) and Hard ST (Yihai Kerry, the same batch of Hard ST used in Example 1) were melted and mixed in a mass ratio of 1:1.2, and the obtained mixed oil was melted and mixed with corn oil in a mass ratio of 2:3 to obtain Oil 1, thereby lowering the melting point of the oil for convenient gavage.

[0376] Oil 2: OCFA algae oil (Yihai Kerry) and high oleic sunflower oil (Yihai Kerry) were melted and mixed at a mass ratio of 1:0.1, and the resulting mixed oil was melted and mixed with corn oil at a mass ratio of 2:3 to obtain Oil 2, thereby lowering the melting point of the oil. (The animal test in this application uses the oil obtained by this preparation method)

[0377] Oil 2 can also be obtained according to the following method: triglyceride of tridecanoic acid, triglyceride of pentadecanoic acid, triglyceride of heptadecanoic acid, DHA algae oil (obtained by refining crude oil purchased from Qingdao Keyuan, the refining method refers to Huang Huaixin's "Optimization of Microalgae DHA Refining Process", crude oil batch MKD120056) and high oleic sunflower oil (Yihai Kerry, the same batch of high oleic sunflower oil used in Example 1) prepared according to the method described in Example 1 are melted and mixed in a mass ratio of 1:46:10:41:2, and the obtained mixed oil is melted and mixed with corn oil in a mass ratio of 2:3 to obtain Oil 2. The melting point of the oil is lowered for easy gavage.

[0378] 3. Fatty acid composition of oil

[0379] The third method "Normalization method" in "GB5009.168-2016 National Food Safety Standard Determination of Fatty Acids in Food" tested the fatty acid composition of Oils 1 and 2, and the results are shown in Table 33.

[0380] Table 33: Major fatty acid composition of oils and fats

[0381]

[0382]

[0383] 4. Animal Experiments

[0384] Experimental animals: 24 pregnant rats were selected for the experiment. A 2×2 factorial experimental design was used. The rats were divided into 4 treatment groups on the 7.5th day of gestation, with 3 replicates in each group and 2 rats in each replicate: 1) CON group; 2) OCFA group; 3) LP group; 4) LP+OCFA group. From the 7.5th day of gestation, the CON group and OCFA group were fed with a normal diet with a protein level of 19%, and fat was gavaged once a day, with a fat gavage dose of 1g / kg / day; the LP group and LP+OCFA group were fed with a low-protein diet with a protein level of 8%, and fat was gavaged once a day, with a fat gavage dose of 1g / kg / day. The daily diet and gavage fat of each group are shown in Table 34. On the 18.5th day of gestation, the rats were slaughtered and sampled for detection and analysis after fasting for 6h. All relevant operation procedures were in accordance with the requirements of the Animal Welfare and Animal Experiment Ethics Committee of China Agricultural University.

[0385] Table 34: Experimental treatment groups

[0386] Grouping Daily Diet Intragastric administration of fat CON Group Normal diet Grease 1 OCFA Group Normal diet Grease 2 LP Group Low protein diet Grease 1 LP+OCFA group Low protein diet Grease 2

[0387] 5. Results

[0388] (1) Effects on glucose metabolism (improving insulin resistance)

[0389] During pregnancy, the placenta produces more substances, including many hormones and cytokines, which will produce resistance to insulin and may affect the effect of insulin. Insulin resistance will be more obvious in the second trimester, and most pregnant women may show insulin resistance during this process. The body can better control blood sugar by producing more insulin. Although a small number of pregnant women produce more insulin, the amount is not enough, which eventually leads to gestational diabetes. Pregnant women with gestational diabetes are prone to macrosomia, fetal malformations, premature births, premature rupture of membranes, and polyhydramnios. In severe cases, it will also increase fetal mortality. The fasting serum glucose (GLU, mmol / L, detected by biochemical analyzer), fasting insulin (INS, μIU / mL, detected by ELISA) and fasting insulin resistance index (HOMA-IR = fasting serum glucose * fasting insulin / 22.5, calculated by referring to Linder, Katarzyna, et al. "Relationships of body composition and liver fat content with insulin resistance in obesity-matched adolescents and adults." Obesity 22.5 (2014): 1325-1331.) of pregnant mice were detected. The results are shown in Table 35 and Fig.29 As shown. Fig.29 It can be seen that compared with the CON group, the insulin resistance index of pregnant mice in the OCFA group showed a downward trend. Compared with the LP group, the insulin resistance index of pregnant mice in the LP+OCFA group decreased significantly. The above results show that odd-numbered fatty acids can help control blood sugar during pregnancy by reducing insulin resistance during pregnancy. It is especially helpful to improve insulin resistance caused by poor diet (low-protein diet). Odd-numbered fatty acids may be beneficial to improve type 2 diabetes.

[0390] Table 35

[0391] CON OCFA LP LP+OCFA Fasting serum glucose (GLU) 3.39 2.81 3.75 2.93 Fasting serum insulin (INS) 11.81 11.18 15.33 8.09 Fasting insulin resistance index 1.79 1.41 2.55 1.05

[0392] (2) Effects on bile acid metabolism (lowering serum bile acid levels)

[0393] Intrahepatic cholestasis of pregnancy is a disease specific to pregnancy, with elevated serum bile acid (TBA, detected by biochemical analyzer) as a specific indicator. This complication can cause fetal distress, premature birth, and increased perinatal mortality. Fig.30It can be seen that compared with the CON group, the serum bile acid of pregnant mice in the OCFA group decreased significantly, which shows that odd-numbered fatty acids have the effect of reducing the serum bile acid of pregnant women. The serum bile acid level of pregnant mice in the LP group was significantly increased compared with the CON group, indicating that poor diet led to abnormal serum bile acid in pregnant mice, which is not conducive to the health of the fetus. After supplementing odd-numbered fatty acids (LP+OCFA group), the serum bile acid of pregnant mice has a downward trend. Intrahepatic cholestasis of pregnancy is generally treated with liver-protecting drugs. Therefore, technicians in this field can foresee that odd-numbered fatty acids, if used in combination with liver-protecting drugs, should have the effect of improving intrahepatic cholestasis of pregnancy caused by poor diet or disease.

[0394] Table 36

[0395] CON OCFA LP LP+OCFA Serum total bile acid (TBA) 5.36 3.76 7.31 6.33

[0396] (3) Liver oxidative stress

[0397] Superoxide dismutase (SOD) is the most important and best free radical scavenger in the body. Glutathione peroxidase (GSH-PX) is an important peroxide decomposing enzyme widely present in the body. It can reduce toxic peroxides into non-toxic hydroxyl compounds, thereby protecting the structure and function of the cell membrane from being disturbed and damaged by peroxides. Malondialdehyde (MDA) is a membrane lipid peroxidation product, and its content can directly reflect the level of cytoplasmic membrane peroxidation. Excessive accumulation of MDA can cause cross-linking and polymerization of macromolecules such as proteins and nucleic acids, leading to changes in the structure and function of cell membranes. Table 37 and Fig.31 The effects of diet and oil treatment on oxidative stress in the liver of pregnant rats are shown. Fig.31 The results showed that compared with the CON group, the liver superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) in the liver of pregnant mice in the OCFA group were significantly increased, and the content of malondialdehyde (MDA) decreased, indicating that odd-numbered fatty acids can reduce the oxidative stress of the liver of mammals in normal diet during pregnancy and improve the body's antioxidant capacity. Compared with the CON group, the liver superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) in the LP group were significantly decreased, and the malondialdehyde (MDA) was significantly increased, indicating that the low-protein diet caused oxidative stress in the liver of pregnant mice, while the liver superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) in the LP+OCFA group were significantly increased, and the content of malondialdehyde (MDA) was significantly decreased, indicating that odd-numbered fatty acids have the effect of reducing the oxidative stress of mammals in pregnancy caused by abnormal diet and improving the body's antioxidant capacity. The above results all show that supplementing odd-numbered fatty acids can reduce the oxidative stress of the liver of mammals during pregnancy.

[0398] Table 37

[0399] CON OCFA LP LP+OCFA Liver superoxide dismutase (SOD) 3.91 4.43 3.14 3.74 Liver glutathione peroxidase (GSH-Px) 44.11 50.16 34.28 39.30 Liver malondialdehyde (MDA) 0.29 0.25 0.42 0.34

[0400] (4) Colon Health

[0401] (i) Histological scoring

[0402] The scoring method is: observe the degree of epithelial cell damage, crypt damage and inflammatory cell infiltration under a microscope, and score them separately. The sum of the three scores is the final score. The results are shown in Table 38. The evaluation method refers to Kim, Janice J., et al. "Investigating intestinal inflammation in DSS-induced model of IBD." Journal of visualized experiments: JoVE 60 (2012).

[0403] Table 38 and Fig.32 The results of mid-colon HE staining showed that the structure of the colon in the LP group was significantly changed compared with the CON group, such as epithelial damage, while the colon damage in the LP+OCFA group was repaired, closer to the CON group. This indicates that the colon histology score of pregnant mice in the LP supplementation group was significantly higher than that in the CON group, indicating that the low-protein diet caused histopathological damage to the colon tissue. The colon histology score of pregnant mice in the LP+OCFA group was significantly lower than that in the LP group, indicating that odd-numbered fatty acids have the effect of improving intestinal histopathological damage induced by abnormal diet or disease.

[0404] Table 38

[0405] CON OCFA LP LP+OCFA Colon tissue injury score of pregnant mice 0.67 0.67 7.83 4.00

[0406] (ii) Intestinal inflammation

[0407] Table 39 and Fig.33 The effects of diet and oil treatment on the gene expression levels of five major inflammatory factors (IL-1β, IL-6, TNF-α, NLRP3 and GSDMD, detected by quantitative PCR) in the colon of pregnant mice were shown. Fig.33As shown, in the normal diet group, dietary supplementation with odd-numbered carbon fatty acids (OCFA group) reduced the expression of IL-1β and GSDMD in colon tissue, suggesting that odd-numbered carbon fatty acids can relieve inflammatory conditions. Compared with the CON group, feeding a low-protein diet (LP group) significantly upregulated the expression of the above five inflammatory factors in the colon, indicating that the low-protein diet exacerbated the inflammatory response of the colon. After supplementing mice fed a low-protein diet with odd-numbered carbon fatty acids (LP+OCFA group), their inflammatory factor levels fell back to the control group or even lower. This shows that odd-numbered carbon fatty acids can play a positive role in alleviating intestinal inflammation. At the same time, existing literature has reported that the high incidence of colorectal cancer is related to certain inflammations of the intestine. Therefore, based on the above experimental results, those skilled in the art can foresee that odd-numbered carbon fatty acids may have a positive effect on inflammatory bowel disease and colorectal cancer.

[0408] Table 39

[0409] CON OCFA LP LP+OCFA Colonic interleukin-1β (IL-1β) 1.01 0.41 1.10 0.06 Colon Interleukin-6 (IL-6) 1.01 1.19 1.90 0.82 Colon tumor necrosis factor-α (TNF-α) 1.02 1.24 2.92 0.40 Colon NLR family pyrin domain-containing protein 3 (NLRP3) 1.00 1.04 1.75 1.12 Colonic Gasdermin D protein (GSDMD) 1.00 0.77 1.09 0.65

[0410] (iii) Intestinal microecology

[0411] Table 40 and Fig.34 The effects of diet and oil treatment on two harmful bacteria in the intestines of pregnant mice are shown. A large number of studies have shown that Helicobacter pylori and Deferrophilus can induce intestinal inflammation. Fig.34 The results showed that for pregnant mice fed a normal diet, supplementation with odd-numbered fatty acids (OCFA group) significantly reduced the abundance of Helicobacter pylori and Deferribacter microorganisms in the feces of pregnant mice (DNA was extracted from feces samples of pregnant mice on the day of slaughter, and 16S rRNA gene sequencing was performed. Shanghai Meiji Biotechnology was commissioned to perform DNA extraction and testing). In mice fed a low-protein diet, supplementation with odd-numbered fatty acids (LP+OCFA group) also reduced the abundance of Deferribacter microorganisms in the intestine. This indicates that odd-numbered fatty acids may have the effect of improving intestinal microecology.

[0412] Table 40

[0413] CON OCFA LP LP+OCFA Intestinal Helicobacter pylori 4.78 1.44 1.63 2.30 Mucispirillum 3.14 0.13 0.81 0.31

[0414] Helicobacter pylori is a common human pathogen that infects about half of the world's population. Helicobacter pylori infection can lead to a series of gastrointestinal diseases of varying degrees, such as chronic gastritis, indigestion, and peptic ulcers. At the same time, Helicobacter pylori is also a clear human carcinogen and an important cause of gastric cancer. Eradication treatment in Helicobacter pylori-infected patients can not only improve gastrointestinal diseases related to it, but also effectively reduce the risk of gastric cancer.

[0415] Antibiotics are currently the conventional treatment for Helicobacter pylori eradication. However, as Helicobacter pylori's antibiotic resistance gradually increases worldwide, the success rate of antibiotic eradication treatment is declining. Moreover, with the rise of intestinal microbiome research, the potential adverse effects of antibiotic treatment (especially repeated long-term use of antibiotics) on intestinal microecology have also attracted widespread attention from the academic community. In order to address these existing problems and challenges, researchers have begun to look for other auxiliary and alternative therapies.

[0416] The results of the present invention suggest that odd-numbered fatty acids may be used as an alternative or auxiliary method for eradicating or treating Helicobacter pylori.

[0417] (5) Nutritional effects

[0418] The ratio of feed consumption to weight gain is the feed-to-meat ratio, also known as feed-to-weight ratio. Fig.35 It can be seen that compared with the CON group, the feed-to-weight ratio of the OCFA group tended to increase. Similarly, compared with the LP group, the feed-to-weight ratio of the LP+OCFA group tended to increase. This indicates that odd-numbered fatty acids are beneficial for controlling the weight of mammals during pregnancy.

[0419] Table 41

[0420] CON OCFA LP LP+OCFA Feed-to-weight ratio (FCR) of pregnant mice during the experimental period 2.38 2.65 2.57 2.96

[0421] Table 42 and Fig.36 The effects of diet and oil treatment on lipid metabolism in pregnant mice (detected using a blood biochemistry kit) are shown. Fig.36 The results show that compared with the CON group, the serum total cholesterol, triglycerides, HDL, and LDL in the low LP group all decreased significantly, indicating that the low-protein diet caused abnormal lipid metabolism in pregnant mice. Compared with the LP group, the LP+OCFA group did not cause a more significant decrease in the above indicators, indicating that dietary supplementation with odd-numbered fatty acids will not have an adverse effect on lipid metabolism in pregnant mammals. At the same time, compared with the CON group in the OCFA group and the LP+OCFA group in the LP group, serum high-density lipoprotein (HDL) was significantly increased. High-density lipoprotein is a plasma lipoprotein that resists atherosclerosis and is a protective factor for coronary heart disease. The above results show that odd-numbered fatty acids can increase serum high-density lipoprotein, improve atherosclerosis, and reduce the risk of coronary heart disease.

[0422] Table 42

[0423] CON OCFA LP LP+OCFA Serum total triglyceride (TG) 2.85 2.95 1.08 0.89 Serum high-density lipoprotein (HDL) 0.84 0.93 0.49 0.61 Serum low-density lipoprotein (LDL) 0.32 0.31 0.22 0.26

[0424] It can be understood from the foregoing that although specific embodiments of the present invention have been described for illustrative purposes, it should be understood that the scope of the present invention is not limited to these specific embodiments. Without departing from the spirit and scope of the present invention, those skilled in the art may make various modifications or improvements to the present invention. These modifications or improvements are all within the scope of protection of the present invention.

Claims

1. Use of odd-numbered fatty acids in the preparation of preparations or medicines for one or more of the following purposes: (1) increasing the protein expression abundance of tight junction-associated proteins (such as Occludin, Claudin and / or ZO-1) in a subject; in particular, increasing the protein expression abundance of the tight junction-associated proteins (such as Occludin, Claudin and / or ZO-1) in the intestine (such as intestinal mucosa), more specifically, the protein expression abundance of tight junction-associated proteins (such as Occludin, Claudin and / or ZO-1) in the duodenum, jejunum and ileum (such as their mucosa); (2) reducing the level of corticotropin-releasing hormone (CRF) in the intestinal tissue of the subject; more preferably, reducing the level of corticotropin-releasing hormone (CRF) in the ileum tissue; (3) Improve or enhance the intestinal mechanical barrier of the subject; improving the intestinal mechanical barrier can defend against the invasion of bacteria, toxins and foreign antigens, maintain the stability of the body's internal environment, and lay the foundation for the absorption of nutrients; (4) increasing the level of immunoglobulins (such as IgG, IgA and / or IgM) in the intestinal tract of the subject; preferably, increasing the level of immunoglobulins (such as IgG, IgA and / or IgM) in the jejunum and ileum; more preferably, increasing the level of immunoglobulins IgG, IgA and / or IgM in the jejunum; more preferably, increasing the level of immunoglobulin A in the ileum; (5) increasing the protein expression abundance of TLR4 and NF-κB in the intestinal tissues of the subjects, especially in the duodenum, jejunum, and ileum; (6) maintaining homeostasis of inflammatory cytokines (such as TNF-α, IL-1β, IL-6, and / or IL-10) in the subject's ileum; (7) increasing the expression of ileal mucin 2 in the subject; (8) Increase the expression of HIF-1α in the intestine and promote the survival of intestinal cells in the intestinal hypoxic environment; (9) Maintaining the immune homeostasis of the subject’s intestine (especially the ileum); (10) increasing the content of nuclear protein Ki-67 in the intestinal tissue of the subject, preferably, the intestinal tissue is the duodenum, jejunum and / or ileum; promoting the proliferation of intestinal epithelial cells of the subject; (11) activating the intestinal mTOR signaling pathway of the subject, increasing the expression of activated mTOR protein in intestinal cells (especially small intestinal cells, such as duodenum, jejunum, and ileum) and / or increasing the level of activated S6 kinase in intestinal cells (especially small intestinal cells, such as duodenum, jejunum, and ileum); (12) increasing the level of digestive enzymes (including but not limited to maltase, aminopeptidase and / or sucrase) in the intestinal tract, especially the small intestine, of the subject, thereby promoting the absorption of nutrients; (13) increasing the level of serotonin in the intestinal tissues (especially the duodenum, jejunum and / or ileum) of the subject and the content of substance P (a neuropeptide) in the ileum, and enhancing the function of the small intestine, such as increasing intestinal motility, promoting gastrointestinal smooth muscle contraction, inhibiting gastric acid and bile secretion, and regulating local gastrointestinal blood flow; (14) promoting intestinal development of a subject; (15) down-regulating the expression of mitophagy-related proteins (such as ULK1, TFEB and / or Parkin) in the intestinal tissue cells (especially the duodenum, jejunum and / or ileum) of the subject to alleviate mitochondrial dysfunction; (16) up-regulating the level of lipid synthesis-related transcription factors (such as PPARγ and / or SREBP-1) in the subject's intestine (especially the small intestine, especially the duodenum and jejunum), and improving the absorption and anabolism of lipids in the intestine (especially the small intestine, especially the duodenum and jejunum); (17) Maintaining energy homeostasis of intestinal cells and improving intestinal energy metabolism; (18) Upregulate the content of type I and type II muscle fibers and the expression of mTOR protein in the muscle tissue of the subjects, while reducing the relative content of AMPK and PGC1-α; (19) improving the energy status of the subject's muscle tissue, promoting cell growth and development, increasing muscle fiber content, inhibiting the conversion of type II muscle fibers to type I muscle fibers, increasing muscle mass, and promoting the overall development of muscle tissue; (20) Upregulating the expression of SREBP-1 in the subject's muscle tissue, promoting lipid anabolism, increasing the uptake and utilization of lipids by muscle tissue, improving energy status, and promoting the development and metabolism of muscle tissue; (21) promoting the development and metabolism of muscle tissue of a subject; (22) Upregulate the expression of activated mTOR in the subject, reduce the expression of Prdm16 and Irisin, inhibit lipolysis, and increase lipid synthesis to promote the development of adipose tissue; (23) Upregulate the levels of SERBP-1 and APOB in the subject’s adipose tissue, increase lipid synthesis in adipose tissue, enhance the body’s transport of lipids, and maintain the energy balance between adipose tissue and the body; (24) promoting the development and metabolism of adipose tissue in a subject; (25) Upregulate the level of GSH-PX in the subject’s serum, improve the body’s overall antioxidant capacity, and maintain overall redox balance; (26) reducing the levels of HIS, jejunal IgE, ileal IgE, jejunal HIS, and ileal HIS in the subject's blood, and reducing the allergic reactions of the body and the jejunum and ileum; (27) reducing allergic reactions in the subject’s body and intestines; (28) Reduce insulin resistance during pregnancy; (29) Control the subject’s blood sugar during pregnancy; (30) Improve insulin resistance caused by poor diet (such as low-protein diet); (31) Prevent gestational diabetes, as well as macrosomia, fetal malformation, premature birth, premature rupture of membranes and / or polyhydramnios caused by gestational diabetes, and reduce fetal mortality; (32) reduce serum bile acid levels during pregnancy; (33) Prevent or improve intrahepatic cholestasis of pregnancy in a subject, such as intrahepatic cholestasis of pregnancy caused by poor diet or disease; reduce the occurrence or risk of fetal distress, premature birth, and perinatal mortality in a subject with intrahepatic cholestasis of pregnancy; (34) increasing the level of superoxide dismutase and glutathione peroxidase in the subject's liver, decreasing the level of malondialdehyde in the subject's liver, and decreasing oxidative stress in the subject during pregnancy; (35) Improving the pathological damage of intestinal tissue induced by abnormal diet or disease; (36) reduce the subject's colon inflammatory factors (such as IL-1β, IL-6, TNF-α, NLRP3 and / or GSDMD) and alleviate intestinal inflammation; (37) Treatment or prevention of inflammatory bowel disease and colorectal cancer; (38) reducing the abundance of Helicobacter pylori and / or Deferribacter in the subject and improving the intestinal microecology; and (39) Preventing or treating diseases caused by Helicobacter pylori, including gastric cancer.

2. The use according to claim 1, characterized in that The application includes the use of odd-numbered carbon fatty acids in the preparation of preparations or medicines for one or more of the following items: (1) increasing the protein expression abundance of the subject's tight junction-associated proteins (such as Occludin, Claudin and / or ZO-1); in particular, increasing the protein expression abundance of the tight junction-associated proteins (such as Occludin, Claudin and / or ZO-1) in the intestine (such as intestinal mucosa), more specifically, the protein expression abundance of the tight junction-associated proteins (such as Occludin, Claudin and / or ZO-1) in the duodenum, jejunum and ileum (such as their mucosa); and (2) reducing the content of corticotropin-releasing hormone (CRF) in the subject's intestinal tissue; thereby improving or enhancing the subject's intestinal mechanical barrier; and / or (4) increasing the content of immunoglobulins (such as IgG, IgA and / or IgM) in the intestinal tract of the subject; preferably, increasing the content of immunoglobulins (such as IgG, IgA and / or IgM) in the jejunum and ileum; more preferably, increasing the content of immunoglobulins IgG, IgA and / or IgM in the jejunum and increasing the content of immunoglobulin A in the ileum; (5) increasing the protein expression abundance of TLR4 and NF-κB in the intestinal tissues of the subject, especially in the duodenum, jejunum and ileum; (6) maintaining the homeostasis of inflammatory cytokines (such as TNF-α, IL-1β, IL-6 and / or IL-10) in the ileum of the subject; (7) increasing the expression of ileal mucin 2 in the subject; and (8) increasing the expression of HIF-1α in the intestine and promoting the survival of intestinal cells in the hypoxic environment of the intestine; thereby maintaining the immune homeostasis of the intestinal tract (especially the ileum) of the subject; and / or (10) increasing the content of nuclear protein Ki-67 in the intestinal tissue of the subject and promoting the proliferation of intestinal epithelial cells of the subject; preferably, the intestinal tissue is the duodenum, jejunum and / or ileum; (11) activating the intestinal mTOR signaling pathway of the subject, increasing the expression of activated mTOR protein in intestinal cells (especially small intestinal cells) and / or increasing the level of activated S6 kinase in intestinal cells (especially small intestinal cells); (12) increasing the level of digestive enzymes (including but not limited to maltase, aminopeptidase and / or sucrase) in the intestinal tract of the subject, especially in the small intestine, and promoting the absorption of nutrients; and (13) increasing the level of serotonin in the intestinal tissue of the subject (especially the duodenum, jejunum and / or ileum) and the content of substance P (a neuropeptide) in the ileum, enhancing the function of the small intestine, such as increasing intestinal motility, promoting gastrointestinal smooth muscle contraction, inhibiting gastric acid and bile secretion, regulating local gastrointestinal blood flow, etc.; thereby promoting the development of the intestinal tract of the subject; and / or (15) down-regulating the expression of mitochondrial autophagy-related proteins (such as ULK1, TFEB and / or Parkin) in the intestinal tissue cells of the subject to alleviate mitochondrial dysfunction; and (16) up-regulating the level of lipid synthesis-related transcription factors (such as PPARγ and / or SREBP-1) in the intestinal tract (especially the small intestine) of the subject to improve the absorption and anabolism of lipids in the intestine (especially the small intestine, especially the duodenum and jejunum); thereby maintaining the energy homeostasis of the intestinal cells of the subject and improving intestinal energy metabolism; and / or (18) upregulating the content of type I and type II muscle fibers and the expression of mTOR protein in the muscle tissue of the subject, while reducing the relative content of AMPK and PGC1-α; (19) improving the energy status of the muscle tissue of the subject, promoting cell proliferation and tissue development, increasing the muscle fiber content, inhibiting the conversion of type II muscle fibers to type I muscle fibers, increasing muscle mass, and promoting the overall development of muscle tissue; and (20) upregulating the expression of SREBP-1 in the muscle tissue of the subject, promoting lipid anabolism, increasing the uptake and utilization of lipids by muscle tissue, improving the energy status, and promoting the development and metabolism of muscle tissue; thereby promoting the development and metabolism of the muscle tissue of the subject; and / or (22) upregulating the expression of activated mTOR in the subject, reducing the expression of Prdm16 and Irisin, inhibiting lipolysis, and increasing lipid synthesis to promote the development of adipose tissue; and (23) upregulating the levels of SERBP-1 and APOB in the adipose tissue of the subject, increasing lipid synthesis in the adipose tissue, enhancing the body's transport of lipids, and maintaining the energy balance between the adipose tissue and the body; thereby promoting the development and metabolism of the adipose tissue of the subject; and / or (25) up-regulating the level of GSH-PX in the subject's serum, thereby increasing the body's overall antioxidant capacity and maintaining overall redox balance; and (26) decreasing the levels of HIS, jejunal IgE, ileal IgE, jejunal HIS, and ileal HIS in the subject's blood, thereby decreasing allergic reactions in the body and the jejunum and ileum; thereby decreasing allergic reactions in the subject's body and intestines; and / or (28) reducing insulin resistance during pregnancy; and (29) controlling blood sugar during pregnancy; thereby preventing gestational diabetes, as well as preventing macrosomia, fetal malformation, premature birth, premature rupture of membranes and / or polyhydramnios caused by gestational diabetes, and reducing fetal mortality; and / or (32) reducing the serum bile acid level of the subject during pregnancy, thereby preventing or improving the subject's intrahepatic cholestasis of pregnancy, such as intrahepatic cholestasis of pregnancy caused by poor diet or disease; and / or, (33) reducing the occurrence or risk of fetal distress, premature birth, and perinatal mortality in the subject with intrahepatic cholestasis of pregnancy; and / or, (34) increasing the level of superoxide dismutase and glutathione peroxidase in the subject's liver, reducing the level of malondialdehyde in the subject's liver, and reducing the subject's oxidative stress during pregnancy, thereby (35) improving the pathological damage to the intestinal tissue induced by abnormal diet or disease in the subject.

3. The use according to claim 1, characterized in that The application includes the use of odd-numbered carbon fatty acids in the preparation of preparations or medicines for one or more of the following items: (3) improving or enhancing the intestinal mechanical barrier of the subject, (9) maintaining the immune homeostasis of the subject's intestine (especially the ileum), (14) promoting the development of the subject's intestine, and (17) maintaining the energy homeostasis of the subject's intestinal cells and improving intestinal energy metabolism; and / or (21) promoting the development and metabolism of muscle tissue in a subject; and / or (24) promoting the development and metabolism of adipose tissue in a subject; and / or (27) Reduce the allergic reaction of the subject's body and intestines.

4. The use according to claim 1, characterized in that The odd-numbered fatty acids are used in the form of free odd-numbered fatty acids and / or in the form of fatty acid chains contained in glycerides such as monoglycerides, diglycerides and / or triglycerides. Preferably, the glycerides are oils and fats; Preferably, the content of C15:0 fatty acid in the odd-numbered fatty acid or glyceride is 80% or more, preferably 85% or more, 90% or more, or 95% or more, based on the total amount of odd-numbered fatty acids; Preferably, the odd-numbered fatty acid or glyceride contains C17:0 in addition to C15:0; the content of C17:0 is ≤18%, ≤13%, ≤5% or ≤3% based on the total weight of the odd-numbered fatty acids.

5. The use according to claim 4, characterized in that The odd-numbered fatty acids are used in the form of oils and fats containing odd-numbered fatty acids; Preferably, in the fatty acid composition of the oil, the content of odd-numbered fatty acids is ≥ 20%, such as 20-70% or 20-60%; Preferably, in the fatty acid composition of the oil: the content of C11:0 fatty acid is not higher than 5%, preferably not higher than 1%, more preferably not higher than 0.5%; the content of C13:0 fatty acid is 1-5%, preferably 2-4%; the content of C15:0 fatty acid is 15-70%, preferably 18-60%; the content of C17:0 fatty acid is 0.1-9%; the content of C19:0 fatty acid is not higher than 5%, preferably not higher than 1%, more preferably not higher than 0.5%; the content of C21:0 fatty acid is not higher than 5%, preferably not higher than 1%, more preferably not higher than 0.5%; the content of C23:0 fatty acid is not higher than 5%, preferably not higher than 1%, more preferably not higher than 0.5%.

6. The use according to claim 5, characterized in that The fatty acid composition of the oil also contains any one of C12:0, C14:0, C14:1, C16:0, C16:1, C18:0, C18:1, C18:2, C20:0, C18:3, C18:3T, C20:1, C20:2, C22:0, C20:3N6, C20:4N6, C20:5N3, C22:1, C20:3N3, C23:0, C22:2, C22:5, C22:6, C24:0 and C24:1 or more; preferably, in the fatty acid composition of the oil, the content of C16:0 is 2-15%, such as 4-13%; the content of C18:0 is ≤5%, such as 0-5% or 0-3%; the content of C18:1 is 5-35%, such as 7-33%; the content of C18:2 is ≤35%, such as 0-35%; the content of C22:5 is ≤5%, such as 0-5% or 1-3.5%; the content of C22:6 is 5-25%, such as 8-22%; the content of other fatty acids does not exceed 1% or is less than 0.5%.

7. The use according to claim 5, characterized in that: In the fatty acid composition of the oil, the content of C13:0 is 1-5%, preferably 2-4%, the content of C15:0 is 40-60%, preferably 45-53%, the content of C16:0 is 1-7%, preferably 3-5.5%, the content of C17:0 is 4-9%, preferably 5-9%, the content of C18:1 is 5-10%, preferably 6-8%, the content of C22:5 is 1-5%, preferably 2-4%, the content of C22:6 is 15-25%, preferably 18-22%; the content of the remaining fatty acids is less than 1% or less than 0.5%; or In the fatty acid composition of the oil, the content of C15:0 is 40-65%, preferably 50-60%, the content of C16:0 is 1-7%, preferably 3-5.5%, the content of C17:0 is 0.1-3%, preferably 0.1-1%, the content of C18:0 is 1-5%, preferably 1-3%, the content of C18:1 is 25-35%, preferably 28-34%, the content of C18:2 is 1-5%, preferably 2-4%; the content of the remaining fatty acids is less than 1% or less than 0.5%; or In the fatty acid composition of the oil, the content of C15:0 is 12-25%, preferably 16-22%, the content of C16:0 is 5-15%, preferably 10-15%, the content of C17:0 is 1-7%, preferably 2-5%, the content of C18:0 is 0.5-3%, preferably 1-2%, the content of C18:1 is 12-22%, preferably 15-20%, the content of C18:2 is 25-35%, preferably 30-35%, the content of C22:6 is 5-15%, preferably 7-12%; the content of other fatty acids is less than 1% or less than 0.5%.

8. The use according to any one of claims 5 to 7, characterized in that: The oil is derived from edible oil, its transesterification product or any combination thereof; Preferably, the edible oil is selected from vegetable oil, microbial oil, animal oil or any combination thereof; Preferably, the vegetable oil comprises one or more of rice oil, sunflower oil (such as high oleic sunflower oil), rapeseed oil, palm oil, palm kernel oil, peanut oil, rapeseed oil, soybean oil, cottonseed oil, safflower seed oil, perilla seed oil, tea seed oil, olive oil, cocoa bean oil, Chinese tallow seed oil, almond oil, apricot kernel oil, tung seed oil, rubber seed oil, corn oil, wheat germ oil, sesame seed oil, castor seed oil, evening primrose seed oil, hazelnut oil, pumpkin seed oil, walnut oil, grape seed oil, borage seed oil, sea buckthorn seed oil, tomato seed oil, macadamia nut oil, coconut oil and cocoa butter, or its fractionation products, self-esterification products or esterification products of two or more oils; Preferably, the animal oil is selected from one or more of lard, chicken fat, sheep fat, fish oil and beef tallow; Preferably, the microbial oil comprises lipids derived from microorganisms, wherein the microorganism is selected from: algae, such as strains of Thraustochytriales, more specifically, Thraustochytriales including Thraustochytrium, Schizochytrium sp. strains; oil-producing bacteria, such as Rhodococcus, such as Rhodococcus opacus); oil-producing yeast, such as Yarrowia, such as Yarrowia lipolytica; mutant strains derived from any of the above strains and mixed strains thereof, preferably, the microorganism is Schizochytrium; Preferably, the weight ratio of odd-numbered fatty acid triglycerides to vegetable oil used for transesterification is 45-70:30-55, 50-65:35-50 or 55-62:38-45.

9. The use according to claim 8, characterized in that: The oil is a chemical esterification product of odd-numbered carbon fatty acid triglyceride, DHA algae oil and high oleic acid sunflower seed oil 234527Z11CNCN exchange product; preferably, in the mixture of odd-numbered carbon fatty acid triglyceride, DHA algae oil and high oleic sunflower oil, the weight ratio of pentadecanoic acid triglyceride to DHA algae oil and high oleic sunflower oil is 40-50:30-45:1-10, such as 40-50:30-40:5-10 or 40-50:38-45:1-5; preferably, in the fatty acid composition of the oil, the content of C15:0 is 12-25%, preferably 16-22%, and the content of C1 The content of C6:0 is 5-15%, preferably 10-15%, the content of C17:0 is 1-7%, preferably 2-5%, the content of C18:0 is 0.5-3%, preferably 1-2%, the content of C18:1 is 12-22%, preferably 15-20%, the content of C18:2 is 25-35%, preferably 30-35%, the content of C22:6 is 5-15%, preferably 7-12%; the content of other fatty acids is less than 1% or less than 0.5%; or The oil is a chemical ester exchange product of odd-numbered fatty acid triglycerides, palm stearin and high oleic sunflower oil; preferably, in the mixture of odd-numbered fatty acid triglycerides, palm stearin and high oleic sunflower oil, the weight ratio of pentadecanoic acid triglyceride to palm stearin and high oleic sunflower oil is 55-62:1-5:35-40; in the fatty acid composition of the oil, the content of C15:0 is 40-65%, preferably 50-60%, the content of C16:0 is 1-7%, preferably 3-5.5%, the content of C17:0 is 0.1-3%, preferably 0.1-1%, the content of C18:0 is 1-5%, preferably 1-3%, the content of C18:1 is 25-35%, preferably 28-34%, the content of C18:2 is 1-5%, preferably 2-4%; the content of other fatty acids is less than 1% or less than 0.5%.

10. A fat as claimed in any one of claims 4 to 9.

11. A preparation comprising the odd-numbered fatty acid or oil as claimed in any one of claims 1 to 9; preferably the preparation is a dietary supplement.

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