Substance and method for improving intestinal health and homeostasis, and nutrition and development of subject

Abstract

Provided are a substance and method for improving intestinal health and homeostasis, and the nutrition and development of a subject. The substance is an odd carbon fatty acid. Specifically, provided is the use of an odd carbon fatty acid in the preparation of a preparation or drug for increasing the protein expression abundance of related tight junction proteins of a subject, reducing the content of a corticotropin-releasing hormone in the intestinal tissue of a subject, improving or enhancing the intestinal mechanical barrier of a subject, maintaining the intestinal immune homeostasis of a subject, promoting the intestinal development of a subject, maintaining the energy homeostasis in intestinal cells of a subject, improving intestinal energy metabolism, promoting the development and metabolism of muscle tissue in a subject, promoting the development and metabolism of adipose tissue in a subject, reducing allergic reactions of the body and the intestinal tract of a subject, reducing the insulin resistance in a pregnant subject, controlling the blood glucose level in a pregnant subject, preventing gestational diabetes mellitus, preventing or improving intrahepatic cholestasis in a pregnant subject, preventing or treating diseases caused by Helicobacter pylori bacteria in a subject, etc.

Description

Materials and methods for improving intestinal health and homeostasis, subject nutrition and development Technical Field

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

[0002] Odd-carbon fatty acids (OCFAs) are a class of fatty acids with an odd number of carbon atoms. OCFAs are found in small amounts in natural lipids and are a normal component of the animal body, undergoing normal metabolism. Prior art generally believes that the accumulation of OCFAs in the human body does not affect normal growth and development.

[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. 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.

[0004] Summary of the Invention

[0005] The present invention aims to develop new applications of odd-numbered carbon fatty acids or triglycerides containing odd-numbered carbon fatty acids.

[0006] Specifically, the present invention provides the use of odd-numbered 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.

[0007] The present invention also provides grease for the above applications.

[0008] The present invention is described in more detail below. BRIEF DESCRIPTION OF THE DRAWINGS

[0009] Figure 1: Differences in the expression levels of multiple tight junction-related proteins in the duodenum, jejunum, and ileum of piglets fed different oil dietary supplements.

[0010] Figure 2: Differences in ileal CRF levels in piglets fed different oil dietary supplements.

[0011] Figure 3: Differences in IgG, IgA, and IgM levels in the jejunum of piglets fed different oil dietary supplements.

[0012] Figure 4: Differences in IgG, IgA, and IgM levels in the ileum of piglets fed different oil-based dietary supplements.

[0013] Figure 5: Differences in TLR4 and NF-κB protein expression levels in the duodenum, jejunum, and ileum of piglets fed different oil dietary supplements.

[0014] Figure 6: Differences in ileum levels of TNF-α, IL-1β, IL-6, and IL-10 in piglets fed different oil-based dietary supplements.

[0015] Figure 7: Differences in the gene expression levels of MUC-2 in the ileum of piglets consuming different oil dietary supplements.

[0016] Figure 8: Differences in Ki67 protein expression levels in the duodenum, jejunum, and ileum of piglets consuming different oil dietary supplements.

[0017] Figure 9: Differences in p-mTOR (phospho-mTOR) protein expression levels in the duodenum, jejunum, and ileum of piglets consuming different oil dietary supplements.

[0018] Figure 10: Differences in p-p70S6K (phospho-p70S6K) protein expression levels in the duodenum, jejunum, and ileum of piglets consuming different oil dietary supplements.

[0019] Figure 11: Differences in the levels of maltase in the duodenum and aminopeptidase N and sucrase in the ileum of piglets fed different oil-based dietary supplements.

[0020] Figure 12: Differences in 5-HT levels in the duodenum, jejunum, and ileum, as well as SP levels in the ileum, among piglets fed different oil dietary supplements.

[0021] Figure 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 that consumed different oil dietary supplements.

[0022] Figure 14: Differences in protein expression levels of PPARγ and SREBP-1 in the duodenum and jejunum of piglets consuming different oil dietary supplements.

[0023] Figure 15: Differences in protein expression levels of MYHC1, MYHC 2a, MYHC 2b, MYHC 2x, mTOR, p-AMPK, and PGC1-α in the dorsal muscle of piglets fed different oil dietary supplements.

[0024] Figure 16: Differences in SREBP-1C gene expression levels in dorsal muscle of piglets fed different oil dietary supplements.

[0025] Figure 17: Differences in protein expression levels of p-mTOR (phospho-mTOR), Prdm16 and Irisin in back fat and p-mTOR and Prdm16 in perirenal fat of piglets fed different oil dietary supplements.

[0026] Figure 18: Differences in gene expression levels of SREBP-1C and APOB in back fat of piglets fed different oil dietary supplements.

[0027] Figure 19: Differences in serum glutathione peroxidase (GSH-PX) levels in piglets fed different oil dietary supplements.

[0028] Figure 20: Differences in IgE and HIS levels in serum, jejunum, and ileum of piglets fed different oil dietary supplements.

[0029] Figure 21: 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).

[0030] Figure 22: Ratio of liver, cerebrum, cerebellum, and brainstem weight to body weight in piglets fed different oil dietary supplements.

[0031] Figure 23: Serum cortisol and adrenocorticotropic hormone (ACTH) levels in piglets fed different oil dietary supplements.

[0032] Figure 24: Serum levels of HDL-C, LDL-C, ALT, AST, TG, and CHOL in piglets fed with different oil dietary supplements.

[0033] Figure 25: Serum TP, ALB, BUN and CREA levels in piglets fed with different oil dietary supplements.

[0034] Figure 26: Serum TNF-α levels in piglets fed with different oil dietary supplements.

[0035] Figure 27: Serum IgG and IgM levels and spleen IgA levels in piglets fed different oil dietary supplements.

[0036] Figure 28: Serum D-LACT levels in piglets fed with different oil dietary supplements.

[0037] Figure 29: Fasting serum glucose (GLU), fasting serum insulin (INS) levels and fasting insulin resistance index of pregnant mice fed different oils and diets.

[0038] Figure 30: Serum bile acid levels in pregnant mice fed different oils and diets.

[0039] Figure 31: Levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and malondialdehyde (MDA) in the liver of pregnant mice fed different oils and diets.

[0040] Figure 32: Colonic histological injury scores and colon HE staining images of pregnant mice that consumed different oils and diets.

[0041] Figure 33: Gene expression levels of colonic inflammatory factors IL-1β, IL-6, TNF-α, NLRP3, and GSDMD in pregnant mice fed different oils and diets.

[0042] Figure 34: The proportion levels of measured sequences of Helicobacter pylori and Deferrogenicobacter in the intestines of pregnant mice that consumed different oils and diets.

[0043] Figure 35: Feed-to-weight ratio of pregnant mice fed different oils and diets during the experimental period.

[0044] Figure 36: Serum TC, TG, HDL, and LDL levels in pregnant mice fed different oils and diets.

[0045] Figure 37: Differences in HIF-1α protein expression levels in the duodenum, jejunum, and ileum of piglets fed different oil dietary supplements.

[0046] Figure 38: Scanning electron micrographs of the intestines of piglets fed different oil dietary supplements.

[0047] Figure 39: HE staining of the intestines of piglets fed with different oil dietary supplements.

[0048] Figure 40: Duodenal villus height, crypt depth and their ratio in piglets fed different lipid dietary supplements.

[0049] Figure 41: Jejunal villus height, crypt depth and their ratio in piglets fed different lipid dietary supplements.

[0050] Figure 42: Ileal villus height, crypt depth and their ratio in piglets fed different lipid dietary supplements.

[0051] In the above figures, * indicates P < 0.05, ** indicates P < 0.01, *** indicates P < 0.005, and ns indicates no significant difference. DETAILED DESCRIPTION

[0052] It should be understood that within the scope of the present invention, the above-mentioned technical features of the present invention and the technical features described in detail below (such as in the examples) 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 ratios between components used in this application are based on weight ratios.

[0053] The present application studies the physiological and medical effects of odd-numbered fatty acids and discovers new biological activities and functions of odd-numbered fatty acids. Therefore, the present application aims to provide new applications of odd-numbered fatty acids.

[0054] 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).

[0055] In some embodiments, in the applications described herein, the content of C15:0 fatty acids is 80% or more, preferably 85% or more, 90% or more, or 95% or more, based on the total weight of odd-numbered fatty acids. In some embodiments, the content of C15:0 fatty acids is 99% or more, based on the total weight of odd-numbered fatty acids. In some embodiments, in the applications described herein, the odd-numbered fatty acids, in addition to C15:0, further contain C17:0; based on the total weight of odd-numbered fatty acids, the content of C17:0 is ≤18%; 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%.

[0056] 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 content of a certain fatty acid 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 the fatty acid in the total amount of odd-numbered fatty acids; and (2) when present in the form of glycerides, the percentage of the fatty acid residue in the total amount of fatty acid residues attached to the glycerides. Unless otherwise indicated, the content herein is expressed in weight or weight percentage.

[0057] 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%. The odd-numbered carbon fatty acid composition of glycerides, especially oils and fats, may 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).

[0058] In the odd-numbered fatty acid composition of glycerides, especially oils and fats, the content of C15:0 fatty acids is greater than 80%, preferably greater than 85%, greater than 90%, or greater than 95%, based on the total weight of odd-numbered fatty acids. In some embodiments, the content of C15:0 fatty acids is greater than 99%, based on the total weight 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%.

[0059] 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%, 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%.

[0060] 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%; and the content of the remaining fatty acids is usually not more than 1% or less than 0.5%.

[0061] In some embodiments, the fatty acid composition of the glyceride, especially the oil, has a C13:0 content of 1-5%, preferably 2-4%, a C15:0 content of 40-60%, preferably 45-53%, a C16:0 content of 1-7%, preferably 3-5.5%, a C17:0 content of 4-9%, preferably 5-9%, a C18:1 content of 5-10%, preferably 6-8%, a C22:5 content of 1-5%, preferably 2-4%, and a C22:6 content of 15-25%, preferably 18-22%; the content of the remaining fatty acids is usually less than 1% or less than 0.5%. In some embodiments, the fatty acid composition of the glyceride, especially the oil, has a C15:0 content of 40-65%, preferably 50-60%, a C16:0 content of 1-7%, preferably 3-5.5%, a C17:0 content of 0.1-3%, preferably 0.1-1%, a C18:0 content of 1-5%, preferably 1-3%, a C18:1 content of 25-35%, preferably 28-34%, and a C18:2 content of 1-5%, preferably 2-4%; the content of the remaining fatty acids is generally less than 1% or less than 0.5%.

[0062] 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%, and the content of C22:6 is 5-15%, preferably 7-12%; the content of the remaining fatty acids is usually less than 1% or less than 0.5%.

[0063] It should be understood that the content of each fatty acid in the fatty acid composition described herein is determined by referring to the third method "normalization method" in "GB5009.168-2016 National Food Safety Standard Determination of Fatty Acids in Food".

[0064] In some embodiments, the grease is derived from an edible oil (e.g., one or more edible oils), an ester exchange product of an edible oil, or any combination thereof. In some embodiments, triglycerides of odd-numbered fatty acids are prepared by ester exchange with conventional edible oils.

[0065] 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 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 one or more of lard, chicken fat, mutton fat, fish oil and beef tallow.

[0066] In some embodiments, the microorganism can be selected from: algae, such as strains of the Thraustochytriales order, more specifically, the Thraustochytriales order includes strains of the genus Thraustochytrium and the genus Schizochytrium sp.; oil-producing bacteria, such as the genus Rhodococcus, such as Rhodococcus opacus; oil-producing yeast, such as the genus Yarrowia, such as Yarrowia lipolytica; mutant strains derived from any of the above strains and mixed strains thereof. Preferably, the microorganism is Schizochytrium.

[0067] Transesterification includes chemical transesterification and enzymatic transesterification. For chemical transesterification, conventional chemical catalysts used for chemical transesterification can be used. Exemplary chemical catalysts include, but are not limited to, acidic 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 used can be 0.1-1.0% of the total weight of the feedstock oil. Chemical catalysts can be used in forms well known in the art. For example, sodium methoxide is typically added to the feedstock oil in solid form, while NaOH and KOH are typically used in aqueous solution, with an exemplary concentration of 30-50%. The amounts described herein refer 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., vacuum degree ≤ 10 mbar) for a period of time (e.g., 0.5 to 1 hour) to uniformly distribute the fatty acids on the glycerol backbone. After the transesterification is completed, the reactants are washed with water.

[0068] When enzymatic transesterification is employed, lipase can be used as a catalyst. The lipase can be lipase powder or immobilized lipase immobilized on a carrier (such as diatomaceous earth, ion exchange resin, etc.). Preferred lipases are those 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. Examples include Lipozyme TL IM and Lopozyme RM from Novozymes, as well as immobilized enzymes or their fermentation broths from AMANO Enzyme Co., Ltd. in Japan. The amount of lipase added is typically between 1 / 10,000 and 10 / 10,000 of the weight of the feedstock oil. Depending on the optimal reaction temperature of the lipase used, the reaction temperature for the pre-transesterification can be within the range of 40-80°C, such as 70±5°C. Similarly, the pre-transesterification process is terminated when the transesterification rate reaches 0.1-1.0%. 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.

[0069] After the transesterification is completed, the obtained transesterified oil can be subjected to conventional refining, such as decolorization and deodorization.

[0070] Glycerides of odd-numbered fatty acids can be prepared by reacting odd-numbered fatty acids with glycerol. For example, an esterification reaction can be carried out between the odd-numbered fatty acids and glycerol in the presence of a lipase. Suitable lipases can be lipases commonly used in the art for esterification reactions, such as the immobilized enzyme NOVO435 (Novozymes). Typically, the molar ratio of the odd-numbered fatty acid to glycerol can be 2 to 5:1. The odd-numbered fatty acid used in the esterification reaction can be a mixture of several odd-numbered fatty acids or a single odd-numbered fatty acid. Typically, after mixing the odd-numbered fatty acids with glycerol, the mixture is heated to 65 to 75°C, followed by addition of 1 to 20%, such as 5 to 15%, of lipase based on the weight of the substrate. The mixture is reacted under a vacuum of ≤10 mbar until the reaction is complete, thereby obtaining the glycerides of odd-numbered fatty acids used in the present invention. The reaction can be carried out under stirring. The obtained glycerides of odd-numbered fatty acids can be purified by molecular distillation.

[0071] The edible oil that is used for transesterification can be various vegetable oils, microorganism oil and animal oil well known in the art, include but not limited to: rice oil, sunflower seed oil (such as high oleic sunflower seed 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 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 theobroma oil one or more.Described animal oil is selected from one or more in lard, chicken fat, mutton fat, fish oil and tallow.Described microorganism oil comprises algae oil.Described edible oil also comprises the transesterification product and the fractionation product of various oils, includes but not limited to the various stearin that fractionation obtains, such as palm stearin.Can select suitable edible oil according to other effect that hopes to obtain. 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.

[0072] During transesterification, an appropriate ratio of odd-numbered triglycerides to vegetable oil can be selected based on 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 triglycerides to vegetable oil can be 45-70:30-55; in some embodiments, the weight ratio of odd-numbered triglycerides to vegetable oil can be 50-65:35-50. In some embodiments, the weight ratio of odd-numbered triglycerides to vegetable oil can be 55-62:38-45.

[0073] 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%, and the content of C22:6 is 5-15%, preferably 7-12%; the content of the remaining fatty acids is usually less than 1% or less than 0.5%.

[0074] In some embodiments, the oil is a chemical transesterification 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. In some embodiments, the fatty acid composition of the oil comprises 40-65%, preferably 50-60%, C16:0 1-7%, preferably 3-5.5%, C17:0 0.1-3%, preferably 0.1-1%, C18:0 1-5%, preferably 1-3%, C18:1 25-35%, preferably 28-34%, and C18:2 1-5%, preferably 2-4%. The content of the remaining fatty acids is generally less than 1% or less than 0.5%.

[0075] The applications of odd-numbered fatty acids described herein include one or more of the following:

[0076] (1) increasing the protein expression abundance of a tight junction-associated protein (such as occludin, claudin, and / or ZO-1) in a subject; in particular, increasing the protein expression abundance of the tight junction-associated protein (such as occludin, claudin, and / or ZO-1) in the intestine (such as the intestinal mucosa), more specifically, 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);

[0077] (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;

[0078] (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 into the body, maintain the stability of the body's internal environment, and lay the foundation for the absorption of nutrients;

[0079] (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;

[0080] (5) increase the protein expression abundance of TLR4 and NF-κB in the intestinal tissues of the subjects, especially in the duodenum, jejunum, and ileum;

[0081] (6) maintaining homeostasis of inflammatory cytokines (such as TNF-α, IL-1β, IL-6, and / or IL-10) in the subject's ileum;

[0082] (7) increasing the expression of ileal mucin 2 in the subject;

[0083] (8) Increase the expression of HIF-1α in the intestine and promote the survival of intestinal cells in the intestinal hypoxic environment;

[0084] (9) Maintaining the immune homeostasis of the subject’s intestine (especially the ileum);

[0085] (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;

[0086] (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);

[0087] (12) increasing the level of digestive enzymes (including but not limited to maltase, aminopeptidase and / or sucrase) in the subject's intestines, especially the small intestine, to promote the absorption of nutrients;

[0088] (13) Increase the level of 5-hydroxytryptamine 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, enhance 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.;

[0089] (14) promoting intestinal development in subjects;

[0090] (15) downregulating 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 subjects to alleviate mitochondrial dysfunction;

[0091] (16) upregulating the levels 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);

[0092] (17) Maintaining energy homeostasis in the subject’s intestinal cells and improving intestinal energy metabolism;

[0093] (18) Upregulate the content of type I and type II myofibers and the expression of mTOR protein in the muscle tissue of the subjects, while reducing the relative content of AMPK and PGC1-α;

[0094] (19) Improve the energy status of the subject's muscle tissue, promote cell growth and development, increase muscle fiber content, inhibit the conversion of type II muscle fibers to type I muscle fibers, increase muscle mass, and promote the overall development of muscle tissue;

[0095] (20) Upregulate the expression of SREBP-1 in the subject's muscle tissue, promote lipid anabolism, increase the uptake and utilization of lipids by muscle tissue, improve energy status, and promote the development and metabolism of muscle tissue;

[0096] (21) Promote the development and metabolism of muscle tissue in subjects;

[0097] (22) Upregulate the expression of activated mTOR, reduce the expression of Prdm16 and Irisin, inhibit lipolysis, increase lipid synthesis and promote the development of adipose tissue;

[0098] (23) Upregulate the levels of SERBP-1 and APOB in the adipose tissue of the subject, increase lipid synthesis in the adipose tissue, enhance the body's transport of lipids, and maintain the energy balance of the adipose tissue and the body;

[0099] (24) promoting the development and metabolism of adipose tissue in a subject;

[0100] (25) Upregulate the GSH-PX content in the subject’s serum, improve the body’s overall antioxidant capacity, and maintain the overall redox balance;

[0101] (26) Reduce the levels of HIS, jejunal IgE, ileal IgE, jejunal HIS, and ileal HIS in the subject's blood, and reduce the allergic reactions of the body and the jejunum and ileum;

[0102] (27) Reduce allergic reactions in the subject’s body and intestines;

[0103] (28) Reduce insulin resistance during pregnancy;

[0104] (29) Control the subject’s blood sugar during pregnancy;

[0105] (30) Improve insulin resistance caused by poor diet (such as low-protein diet);

[0106] (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;

[0107] (32) reduce serum bile acid levels during pregnancy;

[0108] (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;

[0109] (34) increasing the levels of superoxide dismutase and glutathione peroxidase in the subject's liver, decreasing the level of malondialdehyde in the subject's liver, and reducing oxidative stress in the subject during pregnancy;

[0110] (35) Improve the pathological damage of intestinal tissue induced by abnormal diet or disease;

[0111] (36) Reduce the subjects’ colonic inflammatory factors (such as IL-1β, IL-6, TNF-α, NLRP3, and / or GSDMD) and alleviate intestinal inflammation;

[0112] (37) Treatment or prevention of inflammatory bowel disease and colorectal cancer;

[0113] (38) reducing the abundance of Helicobacter pylori and / or Deferrobacter in the subject and improving the intestinal microecology; and

[0114] (39) Preventing or treating diseases caused by Helicobacter pylori, including gastric cancer.

[0115] 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 preparing preparations or drugs for the following purposes:

[0116] (1) increasing the protein expression abundance of a tight junction-associated protein (such as occludin, claudin, and / or ZO-1) in a subject; in particular, increasing the protein expression abundance of the tight junction-associated protein (such as occludin, claudin, and / or ZO-1) in the intestine (such as the intestinal mucosa), more specifically, 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); and

[0117] (2) reduce the level of corticotropin-releasing hormone (CRF) in the subjects' intestinal tissue;

[0118] Thereby improving or enhancing the subject's intestinal mechanical barrier.

[0119] 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 a formulation or medicament for one or more of the following:

[0120] (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;

[0121] (5) increase the protein expression abundance of TLR4 and NF-κB in the intestinal tissues of the subjects, especially in the duodenum, jejunum, and ileum;

[0122] (6) maintaining homeostasis of inflammatory cytokines (such as TNF-α, IL-1β, IL-6, and / or IL-10) in the subject's ileum;

[0123] (7) increasing the expression of ileal mucin 2 in the subject; and

[0124] (8) Increase the expression of HIF-1α in the intestine and promote the survival of intestinal cells in the intestinal hypoxic environment;

[0125] (9) Maintain the immune homeostasis of the subject’s intestine (especially the ileum).

[0126] 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 a formulation or medicament for one or more of the following:

[0127] (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;

[0128] (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);

[0129] (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

[0130] (13) Increase the level of 5-hydroxytryptamine in the intestinal tissues (especially the duodenum, jejunum and / or ileum) and the content of substance P in the ileum, enhance 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.;

[0131] Thereby promoting the intestinal development of the subject.

[0132] 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 a formulation or medicament for one or more of the following:

[0133] (15) downregulating 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

[0134] (16) Upregulating the levels of lipid synthesis-related transcription factors (such as PPARγ and / or SREBP-1) in the subject's intestine (especially the small intestine), thereby improving the absorption and anabolism of lipids in the intestine (especially the small intestine, especially the duodenum and jejunum);

[0135] This maintains the energy homeostasis of the subject's intestinal cells and improves intestinal energy metabolism.

[0136] 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 a formulation or medicament for one or more of the following:

[0137] (18) increasing the content of type I and type II myofibers and the expression of mTOR protein in the subject's muscle tissue, while decreasing the relative content of AMPK and PGC1-α; and / or

[0138] (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

[0139] (20) Upregulate the expression of SREBP-1 in the subject's muscle tissue, promote lipid anabolism, increase the uptake and utilization of lipids by muscle tissue, improve energy status, and promote the development and metabolism of muscle tissue;

[0140] Thereby promoting the development and metabolism of the subject's muscle tissue.

[0141] 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 a formulation or medicament for one or more of the following:

[0142] (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

[0143] (23) Upregulate the levels of SERBP-1 and APOB in the adipose tissue of the subject, increase lipid synthesis in the adipose tissue, enhance the body's transport of lipids, and maintain the energy balance of the adipose tissue and the body;

[0144] Thereby promoting the development and metabolism of the subject's adipose tissue.

[0145] 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 a formulation or medicament for one or more of the following:

[0146] (25) increasing the level of GSH-PX in the subject's serum, improving the body's overall antioxidant capacity, and maintaining overall redox balance; and / or

[0147] (26) Reduce the levels of HIS, jejunal IgE, ileal IgE, jejunal HIS, and ileal HIS in the subject's blood, and reduce the allergic reactions of the body and the jejunum and ileum;

[0148] Thereby reducing the allergic reaction of the subject's body and intestines.

[0149] 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 a formulation or medicament for one or more of the following:

[0150] (28) reducing insulin resistance during pregnancy; and / or

[0151] (29) Control the subject’s blood sugar during pregnancy;

[0152] 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.

[0153] 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 a preparation or medicament for the following purpose: reducing serum bile acid levels in a subject during pregnancy, thereby preventing or improving intrahepatic cholestasis of pregnancy in the subject, such as intrahepatic cholestasis of pregnancy caused by poor diet or disease. 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 a preparation or medicament for the following purpose: reducing the occurrence or risk of fetal distress, premature birth, and perinatal mortality in a subject with intrahepatic cholestasis of pregnancy.

[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 medicines for the following purposes: increasing the levels of superoxide dismutase and glutathione peroxidase in the subject's liver, reducing the level of malondialdehyde in the subject's liver, reducing oxidative stress in the subject during pregnancy, thereby improving the pathological damage to the subject's intestinal tissue induced by an abnormal diet or disease.

[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 colon inflammatory factors in a subject, thereby treating or preventing inflammatory bowel disease and colorectal cancer.

[0156] 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.

[0157] 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 preparing preparations or drugs for the following purposes:

[0158] 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

[0159] Promote the development and metabolism of muscle tissue in a subject; and / or

[0160] Promote the development and metabolism of adipose tissue in a subject; and / or

[0161] Reduces allergic reactions in the subject's body and intestines.

[0162] 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 preparing preparations or drugs for the following purposes:

[0163] Improving intestinal health, preferably, said improving intestinal health includes enhancing intestinal mechanical barrier function, enhancing intestinal immune homeostasis, promoting intestinal development, increasing intestinal digestive enzyme levels, enhancing nutrient absorption, maintaining energy homeostasis of intestinal cells, improving intestinal tissue pathological damage, alleviating intestinal inflammation and / or improving intestinal microecology; and / or

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

[0165] Improve adipose tissue development and metabolism; and / or

[0166] Improve antioxidant capacity or reduce oxidative stress; and / or

[0167] Reduce allergic reactions, preferably reduce intestinal allergic reactions; and / or

[0168] Improve insulin resistance caused by a low-protein diet; and / or

[0169] Improve bile acid metabolism.

[0170] 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 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).

[0171] In some embodiments, the following methods are also provided herein:

[0172] (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 the 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 the mucosa thereof);

[0173] (2) A method for reducing the level of corticotropin-releasing hormone (CRF) in intestinal tissue of a subject; more preferably, a method for reducing the level of corticotropin-releasing hormone (CRF) in ileal tissue;

[0174] (3) methods for improving or enhancing the intestinal mechanical barrier of a subject;

[0175] (4) A method for increasing the level of immunoglobulins (such as IgG, IgA and / or IgM) in the intestine of a subject; preferably, a method for increasing the level of immunoglobulins (such as IgG, IgA and / or IgM) in the jejunum and ileum; more preferably, a method for increasing the level of immunoglobulins IgG, IgA and / or IgM in the jejunum; more preferably, a method for increasing the level of immunoglobulin A in the ileum;

[0176] (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;

[0177] (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;

[0178] (7) a method for increasing the expression of ileal mucin 2 in a subject;

[0179] (8) Methods for increasing the expression of HIF-1α in the intestine to promote the survival of intestinal cells in the intestinal hypoxic environment;

[0180] (9) Methods for maintaining immune homeostasis in the subject's intestine (particularly the ileum);

[0181] (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 in a subject;

[0182] (11) Methods for activating the intestinal mTOR signaling pathway in a subject, increasing the expression of activated mTOR protein in intestinal cells (especially small intestinal cells, such as the duodenum, jejunum, and ileum) and / or increasing the level of activated S6 kinase in intestinal cells (especially small intestinal cells, such as the duodenum, jejunum, and ileum);

[0183] (12) A method for increasing the level of digestive enzymes (including but not limited to maltase, aminopeptidase and / or sucrase) in the intestinal tract, particularly the small intestine, of a subject to promote the absorption of nutrients;

[0184] (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 for 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;

[0185] (14) Methods for promoting intestinal development in a subject;

[0186] (15) A method for alleviating mitochondrial dysfunction by downregulating the expression of mitophagy-related proteins (such as ULK1, TFEB, and / or Parkin) in intestinal tissue cells (especially in the duodenum, jejunum, and / or ileum) of a subject;

[0187] (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);

[0188] (17) Methods for maintaining energy homeostasis in intestinal cells of a subject and improving intestinal energy metabolism;

[0189] (18) A method for upregulating the content of type I and type II myofibers and the expression of mTOR protein in the muscle tissue of a subject, while simultaneously reducing the relative content of AMPK and PGC1-α;

[0190] (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;

[0191] (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;

[0192] (21) Methods for promoting the development and metabolism of muscle tissue in a subject;

[0193] (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;

[0194] (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;

[0195] (24) Methods for promoting the development and metabolism of adipose tissue in a subject;

[0196] (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;

[0197] (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;

[0198] (27) Methods for reducing allergic reactions in the body and intestines of a subject;

[0199] (28) Methods for reducing insulin resistance during pregnancy in a subject;

[0200] (29) Methods for controlling blood sugar during pregnancy;

[0201] (30) Methods to improve insulin resistance caused by poor diet (such as low-protein diet);

[0202] (31) Methods for preventing gestational diabetes mellitus, as well as methods for preventing macrosomia, fetal malformation, premature birth, premature rupture of membranes, and / or polyhydramnios caused by gestational diabetes mellitus, and for reducing fetal mortality;

[0203] (32) Methods for reducing serum bile acid levels in a subject during pregnancy;

[0204] (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, or perinatal mortality in a subject with intrahepatic cholestasis of pregnancy;

[0205] (34) A method for increasing the levels of superoxide dismutase and glutathione peroxidase in a subject's liver, decreasing the level of malondialdehyde in a subject's liver, and reducing oxidative stress in a subject during pregnancy;

[0206] (35) Methods for improving the effects of pathological damage to intestinal tissue induced by abnormal diet or disease in a subject;

[0207] (36) Methods for reducing colonic inflammatory factors (such as IL-1β, IL-6, TNF-α, NLRP3, and / or GSDMD) in a subject to alleviate intestinal inflammation;

[0208] (37) Methods for treating or preventing inflammatory bowel disease and colorectal cancer;

[0209] (38) A method for reducing the abundance of Helicobacter pylori and / or Deferrobacter in a subject to improve the intestinal microecology; and

[0210] (39) A method for preventing or treating a disease caused by Helicobacter pylori in a subject, including gastric cancer; each method comprising 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 free form, in the form of a glyceride (e.g., a monoglyceride, a diglyceride, and / or a triglyceride) of the odd-numbered fatty acid, or in the form of a fat (e.g., 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 the remaining fatty acids is generally less than 1% or less than 0.5%. In some embodiments, the oil is a chemical transesterification 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 piglet intestine; 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 reduce the protein expression abundance of Ki67 in the small intestine, promote the proliferation of intestinal epithelial cells, improve the 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 The results showed that the expression of autophagy-related proteins (including ULK1, TFEB and / or Parkin) in the body was reduced, mitochondrial dysfunction was alleviated, and the energy homeostasis of intestinal cells was maintained; the levels of lipid synthesis-related transcription factors (including PPARγ and / or SREBP-1) were upregulated, the absorption and anabolism of lipids in the small intestine were improved, and the energy homeostasis of intestinal cells was maintained; the content of type I and type II muscle fibers and the expression of mTOR protein in muscle tissue were upregulated, the relative content of AMPK and PGC1-α was reduced, the energy state of muscle tissue was alleviated, cell proliferation and tissue development were promoted, the content of muscle fibers was increased, the transformation of type II muscle fibers to type I muscle fibers was inhibited, the muscle mass was increased, and the overall development of muscle tissue was promoted; the expression of SRE in muscle tissue was upregulated It reduces the expression of SERBP-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 between 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] As used herein, "individual" or "subject" primarily refers to mammals, such as humans, farmed livestock (e.g., pigs, cattle, sheep, horses, camels, donkeys, etc.), research mammals (e.g., rats, mice, gorillas, monkeys, dogs, etc.), and artificially raised or wild animals. This application also does not exclude individuals other than mammals, such as poultry and aquatic species.

[0213] Herein, an effective amount refers to an amount that can achieve the desired purpose after taking it for a period of time. Those skilled in the art can determine the effective amount using conventional methods in the art based on 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 found in conventional dietary supplements, such as dietary fiber, vitamins, minerals, and the like. 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, or feed. The dairy product may be milk powder, liquid milk, milk tablets, yogurt, and the like; the cake may be biscuits, bread, cake, and the like; the beverage may be a carbonated beverage, soda, fruit-flavored water, sour plum soup, bulk low-sugar beverage, mineral water, malted milk, milk tea, coffee, and the like; the cold food may be popsicles, ice cream, ice cream, pudding, and the like.

[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 intended to illustrate the present invention only and are not intended to limit the scope of the invention. The experimental methods in the following examples, for which specific conditions are not specified, are generally 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 experimental process

[0219] The oils listed in the table below are mixed and then chemically transesterified to evenly distribute the fatty acids on the glycerol backbone, eliminating any differences in fatty acid position that could affect digestion, absorption, and function. The resulting oil is refined to create an oil-in-water emulsion. The emulsion is then spray-dried to create a powdered oil. This powdered oil is then fed to piglets as a dietary supplement.

[0220] Piglets are weaned at 7 days old and fed with commercial formula for 6 days. Grease powder is then added to the first feeding each day to dissolve the powder before feeding. The piglets are then fed with commercial formula as normal for the rest of the day for a total of 15 days.

[0221] 2. Preparation of odd-numbered fatty acid triglycerides

[0222] Glycerol (Yihai Kerry) and pentadecanoic acid (purchased from Titan Platform, Adamas, purity ≥95%) were mixed in a molar ratio of 1:4, heated to 70°C and mixed evenly to form the reaction substrate. Immobilized enzyme NOVO435 (Novozymes) was added at 10% of the substrate weight, and the reaction was carried out at 70°C, 300 rpm, and a vacuum of ≤10 mbar for 15 hours to obtain a crude oil product. The crude oil product was separated by molecular distillation, and the heavy phase was pentadecanoic acid glyceride (C15-TAG) with a purity of >98%.

[0223] The above method was used 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.

[0224] 3. Oil Preparation

[0225] Grease 1

[0226] Hard ST (Yihai Kerry, batch RBDHard ST 321, acid value 0.04 mg / KOH / g) and high oleic sunflower oil (Yihai Kerry, model finished grade 1) were melted and mixed uniformly in a mass ratio of 73:27, and then chemically transesterified to uniformly distribute the fatty acids on the glycerol backbone. The chemical transesterification process is as follows: first, vacuum dehydration at 110°C for 1 hour, then addition of sodium methoxide at 0.2% by weight of the oil, vacuum reaction at 110°C for 1 hour, cooling to below 80°C, addition of citric acid at 1.8 times the mass of the sodium methoxide (to make a 10% citric acid solution), stirring, pouring into a separatory funnel, washing with hot water until neutral, and then vacuum dehydration at 110°C. The resulting oil can be refined according to conventional oil refining methods. In this example, the following oil refining method was used to obtain Oil 1.

[0227] Oil refining method:

[0228] 1. Weigh 500g of oil into a 2L glass jacketed reactor and heat naturally until it melts and keep it at 60℃. Stir at 200rpm and fill with nitrogen for protection throughout the process. Detect AV (acid value) and PV (peroxide value).

[0229] 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 5 minutes, stop stirring, let it settle for 4 hours, and after the sedimentation is complete, discard the aqueous phase. Then gradually add water (water addition amount is 15%), stir at 200rpm for 5 minutes, then stop stirring, let it settle for 4 hours; after the sedimentation is complete, discard the aqueous phase.

[0230] 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), the amount of water added (kg) = the amount of alkali added (kg) × 40; prepare alkali solution with water and alkali; and heat the oil to 60 ° C; turn on the stirring at 100 rpm, then add the alkali solution within 5 minutes, stir quickly for 5 minutes after the addition is complete, and let it settle for 4-6 hours; after the sedimentation is completed, discharge the lower aqueous phase; brine washing: add 15% water and 0.5‰ salt, gradually add them dropwise to the algae oil, stir at 100 rpm, stir for 3 minutes, turn off the stirring, settle for 3 hours, and discharge the lower aqueous phase after the sedimentation is completed. Alkaline water washing: Add 15% water and 0.2‰ alkali, gradually add dropwise to the oil, stirring at 100 rpm. Stir for 3 minutes, then turn off stirring, let settle for 3 hours, and after settling, release the lower aqueous phase. Repeat the alkaline water washing twice. Water washing: Add 15% water, stir for 3 minutes, then turn off stirring, let settle for 3 hours, and after settling, release the lower aqueous phase. Wash twice in total.

[0231] 4. Decolorization: Decolorize and deodorize 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 10 mbar. Decolorize for 0.5 hours and then filter.

[0232] 5. Deodorization: temperature is 200℃, vacuum degree is 5mbar, nitrogen is passed through, deodorization time is 2h, and refined oil is obtained after refining.

[0233] Grease 2

[0234] OCFA algae oil (Yihai Kerry) and high oleic sunflower oil (Yihai Kerry) were melted and mixed uniformly in a mass ratio of 92:8. Chemical transesterification was then performed to evenly distribute the fatty acids on the glycerol backbone. The resulting oil was then refined. The chemical transesterification and oil refining methods were the same as for Oil 1 (the oil prepared by this method was used in the animal experiments in this application).

[0235] Oil 2 can also be prepared by the following method: Undecanoic acid triglyceride, tridecanoic acid triglyceride, pentadecanoic acid triglyceride, and heptadecanoic acid triglyceride prepared by the method described above are melted and mixed uniformly with DHA algae oil (obtained by refining crude oil purchased from Qingdao Keyuan; the refining method is based on the "Optimization of Huanghuai New Microalgae DHA Refining Process," crude oil batch MKD120056) and high oleic sunflower oil (Yihai Kerry) in a mass ratio of 1:3:47:7:35:7, followed by chemical transesterification to uniformly distribute the fatty acids on the glycerol backbone. The resulting oil is then refined. The chemical transesterification and oil refining methods are the same as those for Oil 1.

[0236] Grease 3:

[0237] C15-TAG, Hard ST (Yihai Kerry), and high oleic sunflower oil (Yihai Kerry) were melted and mixed uniformly in a mass ratio of 59:4:37, followed by chemical transesterification to evenly distribute the fatty acids on the glycerol backbone. The chemical transesterification and oil refining methods were the same as those for Oil 1.

[0238] 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.

[0239] 4. Fatty acid composition of oil

[0240] The main fatty acid compositions of the above-mentioned 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 Foods". The results are shown in Table 1-1 and Table 1-2, respectively.

[0241] Table 1-1: Main fatty acid composition of Hard ST, high oleic sunflower oil, DHA algae oil and OCFA algae oil

[0242] Table 1-2: Major fatty acid composition of oils 1-3

[0243] 5. Preparation of Oil Dietary Supplement

[0244] 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-mentioned oils 1, 2, and 3) were mixed and stirred at 60°C until dissolved and evenly mixed. 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. The mixture was high-speed sheared at 12,000 rpm for 8 minutes and homogenized twice continuously 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.

[0245] Table 2: Oils and fats used in dietary supplements

[0246] 6. Animal Experiments

[0247] Experimental Animals: Healthy, 7-day-old weaned piglets of the "Du×Chang×Da" strain were randomly assigned to three groups of 10 (see Table 3) based on similar weight, sex, and genetic background. A separate group, G0, consisting of 10 piglets raised on a farm and breastfed from the same source, was also established. Seven-day-old piglets were transferred from the farm to the Institute of Subtropical Medicine, Chinese Academy of Sciences, where they were fed a commercial piglet formula (Tangrenshen) and acclimated. They were managed according to the principles of a large-scale pig farm. After a 6-day pre-feeding period, the supplements described above were added to the basic formula (Tangrenshen) as the first meal of the day. These piglets were fed until 28 days of age, fasted for 12 hours, and then slaughtered for sampling. Samples from eight piglets were collected from each group for analysis. All procedures were in accordance with the Animal Welfare and Animal Experimentation Ethics Committee of the Institute of Subtropical Medicine, Chinese Academy of Sciences.

[0248] Table 3: Experimental treatment groups

[0249] The testing methods for the nutritional parameters mentioned in this article are as follows:

[0250] Serum biochemical parameters were analyzed using commercial kits (Leadman Biotech Limited, Beijing, China) and a biochemical analyzer (Beckman CX4; Beckman Coulter, Germany) to measure total protein (TP), albumin (ALB), blood urea nitrogen (BUN), creatinine (CRE), blood glucose (GLU), and insulin (INS) (fasting insulin resistance index = fasting blood glucose × fasting insulin / 22.5, where fasting blood glucose is expressed in mmol / L and fasting insulin is expressed in μU / mL); immunoglobulins IgG and IgM; and the concentrations of high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (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).

[0251] RT-PCR assays included IL-1β, IL-6, TNF-α, TLR4, NF-κB, and MUC-2 in the duodenum, jejunum, and ileum. SREBP-1C, PPARγ, APOB, FAS, ACC, PPARα, ACOX, CPT-1α, and HSL were detected in the longissimus dorsi muscle and back fat. The RT-QPCR method was based on the protocol described in "B. Song, Dietary leucine supplementation improves intestinal health of mice through intestinal SIgA secretion, 2019."

[0252] Western blot analysis indicators: Ki-67, occludin, claudin, ZO-1, TLR4, NK-κB, mTOR, ULK1, TFEB, SREBP1, PPARγ, HIF1α, PINK, Parkin, and p-mTOR in various intestinal segments; p-mTOR, Prdm16, and irisin in dorsal fat and perirenal fat; Slow MyHC, Fast MyHC, mTOR, AMPK, and PGC-1α in dorsal muscle. Western blot analysis methods were similar to those in "B. Song, Dietary leucine supplementation improves intestinal health of mice through intestinal SIgA secretion, 2019."

[0253] ELISA analysis parameters: Grinded tissues were assayed according to the manufacturer's instructions (Jiancheng Bioengineering Institute, Nanjing, Jiangsu, China). Serum malondialdehyde (MDA), glutathione peroxidase (GSH-PX), and superoxide dismutase (SOD); insulin and glucagon; stress hormones (cortisol and ACTH); D-xylose; IL-1β, IL-6, IL-10, and TNF-α concentrations were measured using a commercial porcine ELISA kit (Cusabio Life Science, Inc., Wuhan, China). IL-1β, IL-6, IL-10, and TNF-α concentrations were measured in each intestinal segment. IgA, IgG, and IgM were measured in the spleen, jejunum, and ileum. Aminopeptidase N, sucrase, and maltase activities were measured in each intestinal segment, as were the expression of serotonin, norepinephrine, substance P, and corticotropin-releasing factor. IgE and HIS were measured in plasma, spleen, and each intestinal segment.

[0254] Intestinal morphology: Referring to “J.Y.Yu, 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 microscopically 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 cold-fixed with 2.5% glutaraldehyde were subjected to scanning and transmission electron microscopy analysis.

[0255] 7. Results

[0256] 7.1 Intestinal Health

[0257] (1) Intestinal mechanical barrier

[0258] Table 4 and Figure 1 show the effects of dietary treatment on the expression of tight junction proteins in the intestine of piglets. As shown in Figure 1, compared with the breast milk group (G0), the G1 group significantly decreased the protein expression abundance of tight junction-associated 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-associated proteins (occludin, claudin, and ZO-1) in the duodenal, jejunal, and ileal mucosa (P < 0.05). Compared with the G1 group, the G2 group also increased the protein expression abundance of tight junction-associated proteins (occludin, claudin, and ZO-1) in the duodenal, jejunal, and ileal mucosa. 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).

[0259] Table 4

[0260] Table 5 and Figure 2 show the effects of dietary treatment on intestinal hormone levels in piglets. Corticotropin-releasing hormone (CRF) is a hormone released in response to stress, primarily promoting the synthesis of adrenocorticotropic hormone (ACH) by the pituitary gland. While CRF is often considered to be secreted solely by the central nervous system, evidence from this study suggests that peripheral CRF release plays a crucial role in regulating gastrointestinal permeability and is part of the gut-brain axis. As shown in Figure 2, compared with the breast milk group (G0), the G1 group significantly increased CRF levels in the ileum of piglets (P < 0.05), suggesting a possible weakening of the mechanical barrier of the terminal small intestine. However, compared with the G1 group, CRF levels in the ileum of piglets in the G3 group were significantly decreased (P < 0.05). CRF levels in the ileum of piglets in the G2 group also decreased compared with the G1 group. These results indicate that dietary supplementation with odd-numbered fatty acids can also enhance or improve the mechanical barrier function of the piglet intestine by reducing the content of CRF in intestinal tissue compared with even-numbered fatty acids.

[0261] Table 5

[0262] (2) Intestinal immune homeostasis

[0263] Table 6-1 and Figure 3 show the effects of dietary treatments on jejunal immunoglobulins in piglets. Immunoglobulins are a class of proteins in the human body that possess antibody activity. They are crucial components of the body's defenses against disease, possessing antibacterial and antiviral properties, enhancing phagocytosis, and, in conjunction with complement, killing or lysing pathogens. IgG, IgM, and IgA are typically measured. 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, while IgM plays a crucial role in early defense. As shown in Figure 3, compared to Group G1, Group G3 showed significant increases in jejunal IgG, IgA, and IgM levels (P < 0.05). Compared to Group G1, Group G2 also showed increases in jejunal IgG and IgM levels. These results suggest that, compared to Group G1, dietary supplementation with odd-numbered fatty acids can maintain jejunal immune homeostasis by increasing jejunal immunoglobulin levels.

[0264] Table 6-1

[0265] Table 6-2 and Figure 4 show the effects of dietary treatment on ileal immunoglobulins in piglets. As shown in Figure 4, compared with the G1 group, the G3 group showed a significant increase in ileal IgA (P < 0.05), while IgG and IgM showed no significant changes. IgA is the first line of defense against pathogen invasion, indicating that dietary supplementation with odd-numbered fatty acids, compared with even-numbered fatty acids, can enhance the jejunum's ability to resist pathogen invasion by increasing the level of immunoglobulin IgA in the ileum, thereby improving jejunal immunity.

[0266] Table 6-2

[0267] Table 7 and Figure 5 show the effects of dietary treatments on the TLR4 / NF-κB signaling pathway in the intestines of piglets. The inflammatory response is an important immune defense mechanism. A normal inflammatory response is a manifestation of immunity and is beneficial to the body. TLR4 / NF-κB is a key inflammatory signaling pathway. Figure 5 shows that compared with the breast milk group (G0), 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 dietary changes led to altered intestinal immune homeostasis. Compared with the G1 group, the G3 group significantly increased the protein expression abundance of TLR4 and NF-κB in the duodenum, jejunum, and ileum (P < 0.05). Compared with the G1 group, the G2 group also increased the protein expression abundance of TLR4 and NF-κB in the duodenum, jejunum, and ileum. These results suggest that compared with even-numbered fatty acids, dietary supplementation with odd-numbered fatty acids can maintain intestinal immune homeostasis by regulating the expression of the TLR4 / NK-κB signaling pathway; the higher the proportion of C15 in the odd-numbered carbon chain fatty acid composition, the more it can maintain intestinal immune homeostasis by regulating the expression of the TLR4 / NK-κB signaling pathway.

[0268] Table 7

[0269] Table 8 and Figure 6 show the effects of dietary treatment on ileal inflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-10) in piglets. Inflammation induces damaged cells to release chemicals, which are generally called inflammatory cytokines. As information molecules between cells, cytokines interact with cells of the immune system, regulate the body's response to disease and infection, and mediate the activities of normal cells in the body. As can be seen from Figure 6, compared with the breast milk group (G0 group), the ileal inflammatory cytokines in the G1 group changed (P < 0.05), indicating that dietary changes lead to changes in ileal immune homeostasis. Compared with G1, the G3 and G2 groups were able to regulate 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 ileal immune homeostasis by regulating inflammatory cytokines.

[0270] Table 8

[0271] Table 9 and Figure 7 show the effects of dietary treatment on ileal mucin-2 levels in piglets. Mucin-2 (MUC-2) is a major component of the intestinal mucus layer, secreted by goblet cells. It forms a gelatinous matrix that accommodates antimicrobial molecules, effectively defending against the invasion of bacteria, viruses, and other pathogens into the intestinal mucosa. As shown in Figure 7, compared with the breast milk group (G0), the expression of ileal mucin-2 in the G1 group was significantly decreased, suggesting a decrease in the immune function of the ileal mucosa (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 dietary supplementation with odd-numbered fatty acids, compared with even-numbered fatty acids, can also maintain the immune homeostasis of the ileum by maintaining the level of mucin in the mucosa.

[0272] Table 9

[0273] Table 10 and Figure 37 show the effects of dietary treatment on the relative expression of the hypoxia-inducible factor (HIF-1α) in the intestinal tract of piglets. The intestinal environment is typically hypoxic. As a major regulator of cellular responses to hypoxia, HIF-1α plays a crucial role in intestinal homeostasis and host-microbe interactions. For example, some of its target genes are involved in intestinal barrier function. As shown in Figure 37, HIF-1α expression was significantly higher in the G3 group than in the G1 group, indicating that dietary supplementation with odd-numbered fatty acids, compared to even-numbered fatty acids, can increase HIF-1α expression in the intestine, thereby promoting intestinal cell survival in the hypoxic environment and benefiting intestinal homeostasis.

[0274] Table 10

[0275] (3) Intestinal development

[0276] Figures 38 to 42 show the results of intestinal development-related tests. Scanning electron microscopy (Figure 38) revealed that the villi of piglets in groups G2 and G3 were longer, thicker, and denser than those in group G1. In particular, the villi in group G3 were comparable to those in group G0. Intestinal HE staining, as shown in Figure 39, showed that the duodenum, jejunum, and ileum of piglets in groups G2 and G3 exhibited improved intestinal morphology compared to group G1, more similar to that of breastfed piglets in group G0. The functional unit of the small intestine is the villus. Longer villi harbor more absorptive cells, while deeper crypts result in less contact between enterocytes and nutrients. Villus height (VH) and the ratio of villus height to crypt depth (CD) (VH:CD) are often used as indicators of small intestinal development. As shown in Figures 40-42, the intestinal VH and VH:CD ratios of piglets in the G1 group were significantly lower than those in the G0 group (both P < 0.05), and the CD ratio was deeper (both P < 0.05), indicating that formula feeding can adversely affect the piglet intestine. As shown in Figure 40 and Table 11-1, in the duodenum, the VH:CD ratios of the G2 and G3 groups were significantly higher than those in the G1 group (P < 0.05). There were no significant differences in VH, CD, or VH:CD ratios between the G2 and G3 groups and those in the G0 group. As shown in Figure 41 and Table 11-2, in the jejunum, the VH:CD ratios of the G2 group were significantly higher than those in the G1 group (P < 0.05), and the CD ratio was significantly lower than that in the G1 group (P < 0.05). The VH and VH:CD ratios of the G3 group were significantly higher than those in the G1 group (P < 0.05), and the CD ratio was significantly lower than that in the G1 group (P < 0.05). These indices were not significantly different from those in the G0 group. As shown in Figure 42 and Table 11-3, in the ileum, the VH:CD ratios of the G2 and G3 groups were significantly higher than those of the G1 group (P < 0.05), while the CD ratios were significantly lower than those of the G1 group (P < 0.05). These indices also approached those of the G0 group. In summary, these results demonstrate that odd-numbered fatty acids improve intestinal morphology, increase VH and VH:CD, and decrease CD, promoting intestinal development and enabling formula-fed animals to achieve intestinal development comparable to that of breastfed animals.

[0277] Table 11-1

[0278] Table 11-2

[0279] Table 11-3

[0280] Table 12 and Figure 8 show the effects of dietary treatment on the proliferation of intestinal epithelial cells in piglets. Ki67 is a proliferating cell-related antigen whose function is closely related to mitosis and is indispensable in cell proliferation. The higher the expression level of Ki67, the more active the cell proliferation. As can be seen from Figure 8, 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 fatty acids, dietary supplementation with odd-numbered fatty acids can improve the intestinal mechanical barrier and promote intestinal development by promoting intestinal epithelial cell proliferation; in the composition of odd-numbered carbon chain fatty acids, the higher the proportion of C15, the more it can improve the intestinal mechanical barrier and promote intestinal development by promoting intestinal epithelial cell proliferation.

[0281] Table 12

[0282] Table 13 and Figure 9 show the effects of dietary treatments on mTOR protein levels in the small intestine of piglets. mTOR (mammalian target of rapamycin) is a kinase that is regulated by growth factors and environmental nutrient levels. It can interact with multiple proteins to activate or inhibit downstream signaling pathways, thereby promoting ribosome formation, protein, lipid, and nucleic acid synthesis, inhibiting autophagy, and promoting cell growth and proliferation. It plays a key role in regulating cellular processes and tissue development. Compared with the breast milk group (G0), the expression of phosphorylated (activated) mTOR protein in the G1 group was significantly reduced (P < 0.05), indicating that normal cell growth activity was inhibited. The G3 group was able to increase the expression of activated mTOR protein in small intestinal cells to or near the level of the breast milk group. In addition, the expression of activated mTOR protein in small intestinal cells of the G2 group was also higher than that of the G1 group. These results indicate that dietary supplementation with odd-numbered fatty acids can activate the mTOR signaling pathway, promoting cell growth and tissue development. A higher proportion of C15 in the odd-numbered fatty acid composition is associated with greater activation of the mTOR signaling pathway, promoting cell growth and tissue development.

[0283] Table 13

[0284] Table 14 and Figure 10 show the effects of treatment on p70S6K levels in the small intestine of piglets. p70S6K (p70 ribosomal S6 kinase) is a protein kinase involved in signal transduction and can be activated by the mTOR protein. It regulates cell proliferation and tissue development by regulating protein synthesis and ribosome biogenesis. Similar to mTOR protein expression, 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 normal cell growth was inhibited. The G3 group was able to increase the level of activated S6 kinase in small intestinal cells to or near the level of the breast milk group. The level of activated S6 kinase in small intestinal cells in the G2 group was also significantly higher than that in the G1 group. This suggests that dietary supplementation with odd-numbered fatty acids can rescue cell proliferation and protein metabolism in small intestinal tissue and promote tissue development. This regulation may be mediated by the mTOR signaling pathway. A higher proportion of C15 in the odd-numbered fatty acid composition is more effective in rescuing cell proliferation and protein metabolism in small intestinal tissue and promoting tissue development.

[0285] Table 14

[0286] Table 15 and Figure 11 show the effects of dietary treatment on small intestinal digestive enzyme levels in piglets. Maltase, aminopeptidase (APN), and invertase are digestive enzymes found in the brush border of the small intestine. They reflect the digestive and absorptive function of the intestine and are important markers of intestinal physiological function and maturation. As shown in Figure 11, compared with the breast milk group (G0), the digestive enzyme levels in the G1 group were significantly different (P < 0.05), indicating that dietary changes led to changes in small intestinal digestive capacity. The G3 group was able to increase small intestinal digestive enzyme levels, reaching or even exceeding those in the breast milk group, indicating that dietary supplementation with odd-numbered fatty acids can enhance the absorption of nutrients by increasing small intestinal digestive enzyme levels.

[0287] Table 15

[0288] Table 16 and Figure 12 show the effects of dietary treatment on the levels of neurotransmitters and neuropeptides in the small intestine of piglets. 5-HT is a monoamine neurotransmitter primarily synthesized in chromaffin cells in the small intestine, with smaller amounts also found in platelets and the central nervous system. It exerts distinct functions in different tissues. Approximately 90% of 5-HT in the animal body is present in gastrointestinal cells and the myenteric plexus, where it participates in the regulation of intestinal motility. Substance P (SP) is also widely distributed in the gastrointestinal tract, primarily promoting gastrointestinal smooth muscle contraction, 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 levels of neurotransmitters and neuropeptides in the small intestine of the G1 group were similar or slightly lower. However, the G3 group could significantly increase the levels of serotonin 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 serotonin in the duodenum, suggesting that dietary supplementation of odd-numbered fatty acids can enhance the function of the small intestine by increasing the levels of gut-brain peptides related to the gut-brain axis.

[0289] Table 16

[0290] (4) Intestinal energy metabolism

[0291] Table 17 and Figure 13 show the effects of dietary treatment on the level of mitophagy in the small intestine of piglets. Mitophagy is the process of programmed degradation of mitochondria in cells, which often occurs in damaged or defective mitochondria and is used to prevent the accumulation of dysfunctional mitochondria and the resulting cell abnormalities. As shown in Figure 13, 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 cells. The G2 and G3 groups were able to downregulate the expression levels of intracellular mitophagy-related proteins to levels similar to those of the breast milk group, indicating that compared with even-numbered fatty acids, dietary supplementation with odd-numbered fatty acids can alleviate mitochondrial dysfunction and help maintain the energy homeostasis of intestinal cells; in the composition of odd-numbered 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.

[0292] Table 17

[0293] Table 18 and Figure 14 show the effects of dietary treatments on lipid metabolism in the small intestine of piglets. Lipids are important functional substances within the body and cells and serve as the primary form of energy storage. The activity of lipid metabolism reflects the overall energy status of a tissue. PPARγ and SREBP-1 are transcription factors involved in lipid metabolism in cells and are closely linked to lipid uptake and synthesis. As shown in the figure above, compared with the breast milk group (G0), the levels of PPARγ and SREBP-1 in the duodenum and jejunum of the G1 group were significantly lower (P < 0.05), indicating that lipid synthesis was inhibited and cellular energy status was abnormal. The G2 and G3 groups upregulated the levels of lipid synthesis-related transcription factors, reaching or approaching the levels of the breast milk group. This suggests that dietary supplementation with odd-numbered fatty acids can enhance lipid absorption and anabolism in the small intestine of piglets, thereby maintaining energy homeostasis in intestinal cells. A higher proportion of C15 in the odd-numbered fatty acid composition enhances lipid absorption and anabolism in the small intestine of piglets, thereby maintaining energy homeostasis in intestinal cells.

[0294] Table 18

[0295] (5) Development and metabolism of muscle tissue

[0296] Muscle tissue is composed of muscle fibers (cells), which can be further divided into type I (MYHC I) and type II (MYHC II) fibers based on their appearance and function. Type I fibers, also known as red muscle fibers, slow-twitch fibers, or slow-oxidative fibers, contract slowly, have low force, utilize oxygen well, and possess superior endurance. Type II fibers, known as white muscle fibers, fast-twitch fibers, or fast-glycolytic fibers, primarily generate short-term energy through glycolysis. They have poor endurance, but significantly enhance explosive power and speed during exercise and are a primary determinant of muscle strength and speed. Fast-twitch fibers also have a thicker cross-sectional area, and muscle tissue rich in fast-twitch fibers tends to develop and grow larger. In animal nutrition, the number of fast-twitch fibers is significantly correlated with meat production, making it a key indicator of animal production. mTOR also plays a crucial role in muscle tissue, controlling skeletal muscle anabolic and catabolic signals, thereby regulating muscle growth and 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.

[0297] As shown in Table 19 and Figure 15, compared with the breast milk group (G0), the G1 group showed a significant decrease in the content of type I and type II myofibers and mTOR protein expression in the dorsal muscle tissue (P < 0.05), while the levels of AMPK and PGC1-α increased significantly (P < 0.05). This suggests that the muscle tissue of the G1 piglets is in a state of energy deficiency, with slowed cell proliferation and a continuous conversion of type II to type I myofibers, leading to muscle loss. The G3 group significantly increased the content of type I and type II myofibers and mTOR protein expression in muscle tissue (P < 0.05), while simultaneously decreasing the relative levels of AMPK and PGC1-α (P < 0.05). The G2 group also increased the content of type I and type II myofibers and mTOR protein expression in muscle tissue, while decreasing the relative levels 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 composition of odd-numbered carbon chain fatty acids, 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.

[0298] Table 19

[0299] Muscle is the main target organ for energy metabolism and glycolipid metabolism in the body, and there is an active lipid metabolism process, especially during exercise. SREBP-1 is a transcription factor related to lipid metabolism in cells, and is closely related to the uptake and synthesis of lipids. As shown in Table 20 and Figure 16, compared with the breast milk group (G0 group), the content of SREBP-1 in the G1 group decreased to a certain extent, but not significantly. However, the G2 and G3 groups were able to significantly increase the expression of SREBP-1 in muscle tissue, indicating that there is more active lipid anabolism in muscle tissue. This shows that dietary supplementation with odd-numbered 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 echo the above-mentioned increase in muscle cell proliferation and muscle mass.

[0300] Table 20

[0301] (6) Development and metabolism of adipose tissue

[0302] Similar to the other tissues mentioned above, the mTOR protein is a crucial component of lipid production and maintenance in adipose tissue, as well as its development. The 16PR domain-containing transcription factor (Prdm16) and irisin can act on white adipocytes, inducing their conversion to brown adipocytes. Although the amount of brown adipose tissue in adults is low, its heat production efficiency is extremely high; a small amount of brown fat can burn a significant amount of calories. Activated brown adipose tissue generates heat by rapidly consuming glucose and fat, making it crucial for combating obesity. Therefore, Prdm16 and irisin are the molecular switches for the browning of white fat, associated with lipolysis. Early in animal development, a certain amount of fat storage plays a crucial role in the body's overall energy metabolism and homeostasis. As shown in Table 21 and Figure 17, compared with the breast milk group (G0), the levels of activated mTOR protein in the back fat and perirenal fat of piglets in the G1 group were significantly reduced (P < 0.05), while Prdm16 and Irisin were significantly increased (P < 0.05), indicating that lipid synthesis and adipose tissue development were inhibited, and the browning process of white fat was accelerated, with significant lipolysis. The G2 and G3 groups were able to significantly upregulate the expression of activated mTOR and reduce the expression of Prdm16 and Irisin, indicating that dietary supplementation with odd-numbered fatty acids can inhibit lipolysis while increasing lipid synthesis and promoting adipose tissue development; the higher the proportion of C15 in the odd-numbered fatty acid composition, the more it can inhibit lipolysis and increase lipid synthesis and promote adipose tissue development.

[0303] Table 21

[0304] Similarly, SREBP-1 is a transcription factor related to lipid metabolism in cells and is closely related to the uptake and synthesis of lipids. APOB (apolipoprotein) is the main component of lipoproteins and is responsible for the transport of lipids in various systems. As shown in Table 22 and Figure 18, 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 increased 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 fatty acids can increase lipid synthesis in adipose tissue and enhance the body's transport of lipids, which helps maintain energy balance between adipose tissue and the body.

[0305] Table 22

[0306] (7) Body redox state

[0307] Glutathione peroxidase (GSH-PX) is a type of enzyme with peroxidase activity that plays a detoxifying role in organisms. Its main biological function is to reduce lipid peroxides to corresponding alcohols and to reduce free hydrogen peroxide to water, which has antioxidant properties. As shown in Table 23 and Figure 19, compared with the breast milk group (G0 group), the GSH-PX content of piglets in the G1 group was significantly reduced, which means that the body's 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 piglet serum 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.

[0308] Table 23

[0309] (8) Allergic reactions of the body and intestines

[0310] The stronger the allergic reaction, the greater the release of IgE and HIS. As shown in Table 24 and Figure 20, G3 significantly reduced blood HIS (P < 0.05), jejunal IgE (P < 0.05), ileal IgE (P < 0.05), and HIS (P < 0.05) compared to G1. Jejunal and ileal IgE also decreased in the G2 group compared to the G1 group. This suggests that dietary supplementation with odd-numbered fatty acids, compared to even-numbered fatty acids, is beneficial in reducing allergic reactions in the body and in the jejunum and ileum.

[0311] Table 24

[0312] (10) Nutritional effects

[0313] 4.1 Growth performance

[0314] As shown in Table 25 and Figure 21, dietary supplementation with odd-numbered fatty acids did not significantly affect the average daily gain, average daily feed intake, and feed weight of piglets.

[0315] Table 25

[0316] As shown in Table 26 and Figure 22, dietary supplementation with odd-numbered fatty acids did not affect the weights of the liver, cerebrum, cerebellum, and brainstem in piglets.

[0317] Table 26

[0318] During the experimental period, the feces of the piglets were observed every day, and it was found that the piglets had no obvious diarrhea and were in good growth condition throughout the whole process, indicating that dietary supplementation of odd-numbered fatty acids would not cause diarrhea in piglets.

[0319] Individual nonspecific reactions to various stressful stimuli (stressors) are called stress responses, and long-term stress responses can lead to symptoms. When the body undergoes an emergency response, blood levels of cortisol and adrenocorticotropic hormone (ACTH) increase. As shown in Table 27 and Figure 23, there were no significant differences (P>0.05) in blood stress hormones (cortisol and ACTH) between the G1 and G3 groups, nor were there significant differences with the G2 group, indicating that dietary supplementation with odd-numbered fatty acids did not induce a stress response in lactating piglets.

[0320] Table 27

[0321] Abnormal lipid metabolism can lead to elevated triglycerides (TG), cholesterol (CHOL), and low-density lipoprotein (LDL-C) in the blood, decreased high-density lipoprotein (HDL-C), and liver damage (liver damage can lead to elevated aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in the blood). As shown in Table 28 and Figure 24, there were no significant differences in TG, CHOL, HDL-C, and LDL-C levels between the G1, G2, and G3 groups. There were also no significant differences in AST and ALT levels. This suggests that dietary supplementation with odd-numbered fatty acids does not lead to abnormal lipid metabolism compared to even-numbered fatty acids.

[0322] Table 28

[0323] Table 29 and Figure 25 show the effects of dietary treatments on blood protein metabolism-related indicators in piglets. Figure 25 shows that dietary supplementation with odd-numbered fatty acids did not affect blood protein metabolism.

[0324] Table 29

[0325] TNF-α is a cytokine involved in systemic inflammation, primarily secreted by macrophages. It can trigger an acute phase reaction, promote fever, and induce apoptosis. Serum TNF-α levels can, to a certain extent, serve as an indicator of overall inflammatory status. Table 30 and Figure 26 show the effects of dietary treatments on key serum inflammatory markers in piglets. Figure 26 shows that dietary supplementation with odd-numbered fatty acids did not impose an additional burden on overall inflammatory status in piglets compared to the G0 and G1 groups.

[0326] Table 30

[0327] Table 31 and Figure 27 show the effects of the dietary treatments on immunoglobulins in the blood and spleen of piglets. As can be seen, there were no significant differences in IgG and IgM levels in the blood, nor in IgA levels in the liver, between the G2 and G3 groups and the G1 group. This suggests that dietary supplementation with odd-numbered fatty acids, compared with even-numbered fatty acids, did not result in significant changes in humoral immunity.

[0328] Table 31

[0329] D-lactic acid (LACT) is a metabolic end product of indigenous gastrointestinal bacteria. Mammals lack the enzymes to rapidly metabolize it, so increased D-lactic acid levels in the blood can reflect changes in intestinal permeability. Figure 28 shows the effects of dietary treatment on D-lactic acid levels in piglet blood. Table 32 and Figure 28 show that serum D-lactic acid levels in piglets in the G2 and G3 groups were not significantly different from those in the G1 group, indicating that dietary supplementation with odd-numbered fatty acids did not result in significant changes in intestinal permeability compared to even-numbered fatty acids.

[0330] Table 32

[0331] Example 2

[0332] 1. Basic experimental process

[0333] In this study, pregnant rats were fed a normal diet and a low-protein diet (an abnormal diet) containing or without OCFA oils. (Hard ST and high-oleic sunflower oil were used to eliminate the effects of OCFA algae oil on the ratio of DHA, SFA, UFA, and n-3 to n-6 unsaturated fatty acids.) The rats were gavaged starting on gestational day 7.5. After a 6-hour fast from gestational day 18.5, the rats were anesthetized with ether and sacrificed for sampling.

[0334] Unless otherwise stated, the various detection methods of this example are the same as those of Example 1.

[0335] 2. Oil Preparation

[0336] Oil 1: DHA algae oil (crude oil purchased from Qingdao Keyuan and refined, 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 resulting 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 to facilitate gavage.

[0337] Oil 2: OCFA algae oil (Yihai Kerry) and high oleic sunflower oil (Yihai Kerry) were melted and mixed uniformly at a mass ratio of 1:0.1. The resulting mixture was then melted and mixed uniformly with corn oil at a mass ratio of 2:3 to produce Oil 2, thereby lowering the melting point of the oil. (The animal experiments in this application used oil prepared using this method.)

[0338] Oil 2 can also be prepared according to the following method: triglyceride tridecanoate, triglyceride pentadecanoate, triglyceride heptadecanoate, DHA algae oil (crude oil purchased from Qingdao Keyuan and refined, 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 to facilitate gavage.

[0339] 3. Fatty acid composition of oil

[0340] 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.

[0341] Table 33: Major fatty acid composition of oils and fats

[0342] 4. Animal Experiments

[0343] Experimental Animals: Twenty-four pregnant female mice were enrolled in a 2×2 factorial design. On gestational day 7.5, the females were divided into four treatment groups, with three replicates per group and two females per replicate: 1) CON group; 2) OCFA group; 3) LP group; and 4) LP+OCFA group. Starting on gestational day 7.5, the CON and OCFA groups were fed a normal diet containing 19% protein and received daily oral administration of 1 g / kg / day of oil. The LP and LP+OCFA groups were fed a low-protein diet containing 8% protein and received daily oral administration of 1 g / kg / day of oil. The dietary and oral administration oil content of each group is shown in Table 34. On gestational day 18.5, the females were fasted for 6 hours and sacrificed for sampling and analysis. All procedures were in accordance with the Animal Welfare and Animal Experimentation Ethics Committee of China Agricultural University.

[0344] Table 34: Experimental treatment groups

[0345] 5. Results

[0346] (1) Effects on glucose metabolism (improving insulin resistance)

[0347] During pregnancy, the placenta produces a large number of substances, including hormones and cytokines, which can cause resistance to insulin and potentially affect its effects. Insulin resistance becomes more pronounced during the second trimester, and most pregnant women experience this during this period. This can help control blood sugar levels by increasing insulin production. However, in a small number of pregnant women, although insulin production increases, it is insufficient to meet the required levels, ultimately leading to gestational diabetes. Pregnant women with gestational diabetes are more likely to develop macrosomia, fetal malformations, premature birth, premature rupture of membranes, and polyhydramnios. In severe cases, this can 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 with reference 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 tested. The results are shown in Table 35 and Figure 29. As can be seen from Figure 29, 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 indicate that odd-numbered carbon fatty acids can help control blood sugar during pregnancy by reducing insulin resistance during pregnancy. It is especially beneficial to improve insulin resistance caused by a poor diet (low-protein diet). Odd-numbered carbon fatty acids may be beneficial to improving type 2 diabetes.

[0348] Table 35

[0349] (2) Effects on bile acid metabolism (reducing serum bile acid levels)

[0350] Intrahepatic cholestasis of pregnancy is a condition specific to pregnancy, characterized by elevated serum bile acids (TBA, measured by biochemical analyzer). This complication can lead to fetal distress, premature birth, and increased perinatal mortality. As shown in Table 36 and Figure 30, compared with the CON group, serum bile acid levels in pregnant mice in the OCFA group were significantly lower, demonstrating the effectiveness of odd-numbered fatty acids in lowering serum bile acid levels in pregnant mice. Serum bile acid levels in pregnant mice in the LP group were significantly higher than in the CON group, suggesting that a poor diet leads to abnormal serum bile acid levels in pregnant mice, which is detrimental to fetal health. Supplementation with odd-numbered fatty acids (LP+OCFA group) showed a downward trend in serum bile acid levels in pregnant mice. Intrahepatic cholestasis of pregnancy is generally treated with hepatoprotective drugs. Therefore, those skilled in the art would anticipate that the combination of odd-numbered fatty acids and hepatoprotective drugs would be effective in improving intrahepatic cholestasis of pregnancy caused by poor diet or disease.

[0351] Table 36

[0352] (3) Liver oxidative stress

[0353] Superoxide dismutase (SOD) is the most important and optimal free radical scavenger in the body. Glutathione peroxidase (GSH-PX) is a widely present, important peroxide-degrading enzyme that reduces toxic peroxides into non-toxic hydroxyl compounds, thereby protecting the structure and function of cell membranes from peroxide interference and damage. Malondialdehyde (MDA) is a membrane lipid peroxidation product, and its level directly reflects the level of plasma membrane peroxidation. Excessive accumulation of MDA can cause cross-linking and polymerization of macromolecules such as proteins and nucleic acids, leading to changes in cell membrane structure and function. Table 37 and Figure 31 show the effects of diet and oil treatment on oxidative stress in the livers of pregnant mice. Figure 31 shows that compared with the CON group, the livers of pregnant mice fed OCFA showed significantly increased superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), while the MDA level decreased. This suggests that odd-numbered fatty acids can reduce oxidative stress in the livers of pregnant mammals fed a normal diet and enhance the body's antioxidant capacity. Compared with the CON group, the LP group showed significantly decreased liver superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), and significantly increased malondialdehyde (MDA), indicating that the low-protein diet caused oxidative stress in the livers of pregnant mice. In the LP+OCFA group, compared with the LP group, liver superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), and malondialdehyde (MDA) levels were significantly decreased, indicating that odd-numbered fatty acids can reduce oxidative stress in pregnant mammals caused by an abnormal diet and enhance the body's antioxidant capacity. These results indicate that odd-numbered fatty acid supplementation can reduce oxidative stress in the livers of pregnant mammals.

[0354] Table 37

[0355] (4) Colon health

[0356] (i) Histological scoring

[0357] Scoring was performed by microscopically observing the extent of epithelial cell damage, crypt damage, and inflammatory cell infiltration, and scoring each separately. The sum of these three scores constituted the final score. The results are shown in Table 38. The evaluation method was based on Kim, Janice J., et al. "Investigating intestinal inflammation in a DSS-induced model of IBD." Journal of visualized experiments: JoVE 60 (2012).

[0358] The colon HE staining results in Table 38 and Figure 32 show that the LP group exhibited significant structural changes in the colon, including epithelial damage, compared to the CON group. However, the LP+OCFA group showed repaired colonic damage, closer to that of the CON group. This suggests that the LP-supplemented group showed significantly higher colon histological scores than the CON group, indicating that the low-protein diet caused pathological damage to colon tissue. The LP+OCFA group also showed significantly lower colon histological scores than the LP group, demonstrating that odd-numbered fatty acids can improve intestinal pathological damage induced by an abnormal diet or disease.

[0359] Table 38

[0360] (ii) Intestinal inflammation

[0361] Table 39 and Figure 33 show 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) in the colon of pregnant mice (quantitative PCR analysis). As shown in Figure 33, dietary supplementation with odd-numbered fatty acids (OCFA group) reduced the expression of IL-1β and GSDMD in colon tissue in the normal diet group, suggesting that odd-numbered fatty acids can alleviate inflammation. Compared with the CON group, feeding the low-protein diet (LP group) significantly increased the expression of these five inflammatory factors in the colon, indicating that the low-protein diet exacerbated the inflammatory response in the colon. However, supplementation of mice fed the low-protein diet with odd-numbered fatty acids (LP+OCFA group) reduced the levels of these inflammatory factors to levels even lower than those in the control group. This suggests that odd-numbered fatty acids can play a positive role in alleviating intestinal inflammation. Furthermore, literature has reported that the high incidence of colorectal cancer is associated with certain intestinal inflammations. Therefore, based on these experimental results, those skilled in the art can foresee that odd-numbered fatty acids may have a positive effect on inflammatory bowel disease and colorectal cancer.

[0362] Table 39

[0363] (iii) Intestinal microecology

[0364] Table 40 and Figure 34 show the effects of diet and oil treatment on two harmful bacteria in the intestines of pregnant mice. A large number of studies have shown that Helicobacter pylori and Deferrophilus can induce intestinal inflammation. Figure 34 shows that for pregnant mice fed a normal diet, supplementation with odd-numbered fatty acids (OCFA group) significantly reduced the abundance of Helicobacter pylori and Deferrophilus microorganisms in the feces of pregnant mice (fecal samples of pregnant mice were taken on the day of slaughter for DNA extraction and 16S rRNA gene sequencing, and Shanghai Meiji Biological 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 Deferrophilus microorganisms in the intestine. This shows that odd-numbered fatty acids may have the effect of improving intestinal microecology.

[0365] Table 40

[0366] Helicobacter pylori is a common human pathogen, infecting approximately half of the world's population. H. pylori infection can lead to a range of gastrointestinal disorders, including chronic gastritis, dyspepsia, and peptic ulcers. It is also a known human carcinogen and a major cause of gastric cancer. Eradication therapy in patients infected with H. pylori not only improves associated gastrointestinal symptoms but also effectively reduces the risk of gastric cancer.

[0367] Antibiotics are currently the standard treatment for Helicobacter pylori eradication. However, with the increasing global prevalence of antibiotic resistance in Helicobacter pylori, the success rate of antibiotic eradication therapy is declining. Furthermore, with the rise of gut microbiome research, the potential adverse effects of antibiotic therapy (especially repeated, long-term antibiotic use) on the gut microbiome have attracted widespread attention. To address these existing problems and challenges, researchers have begun to explore other complementary and alternative therapies.

[0368] 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.

[0369] (5) Nutritional effects

[0370] The feed-to-meat ratio, also known as the feed-to-weight ratio, is the ratio of feed consumption to weight gain. Table 41 and Figure 35 show that the feed-to-weight ratio of the OCFA group increased compared to the CON group. Similarly, the feed-to-weight ratio of the LP+OCFA group increased compared to the LP group. This suggests that odd-numbered fatty acids are beneficial for controlling weight gain during pregnancy in mammals.

[0371] Table 41

[0372] Table 42 and Figure 36 show the effects of diet and oil treatment on lipid metabolism in pregnant mice (measured using a blood biochemistry kit). Figure 36 shows that compared to the CON group, the low-protein diet group showed significant decreases in serum total cholesterol, triglycerides, HDL, and LDL, indicating that the low-protein diet caused abnormal lipid metabolism in pregnant mice. The LP+OCFA group did not show a more significant decrease in these indicators compared to the LP group, indicating that dietary supplementation with odd-numbered fatty acids does not adversely affect lipid metabolism in pregnant mammals. Furthermore, the OCFA group showed a significant increase in serum high-density lipoprotein (HDL) compared to the CON group, and the LP+OCFA group showed a significant increase in serum high-density lipoprotein (HDL). HDL is an anti-atherosclerotic plasma lipoprotein and a protective factor against coronary heart disease. These results demonstrate that odd-numbered fatty acids can increase serum HDL, improve atherosclerosis, and reduce the risk of coronary heart disease.

[0373] Table 42

[0374] It will be appreciated 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. Various modifications or improvements may be made to the present invention by those skilled in the art without departing from the spirit and scope of the present invention. Such modifications or improvements are 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) Upregulating the levels 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 the subject, and improving the intestinal tract (especially the small intestine, especially the duodenum and jejunum) Absorption and anabolism of lipids in the intestine; (17) Maintaining the energy homeostasis of the intestinal cells of the subject 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) Upregulates the expression of activated mTOR, reduces the expression of Prdm16 and Irisin, and inhibits lipolysis. (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 allergic reactions in 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 selected from algae, such as strains of the Thraustochytriales order, more specifically, the Thraustochytriales order includes the genus Thraustochytrium, Schizochytrium sp. strains; oleaginous bacteria, such as Rhodococcus, such as Rhodococcus opacus); oleaginous yeast, such as Yarrowia, such as Yarrowialipolytica; mutant strains derived from any of the above strains and mixed strains thereof, preferably, the microorganism is Schizochytrium sp.; 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 ester exchange product of odd-numbered carbon fatty acid triglycerides, DHA algae oil and high oleic sunflower oil; preferably, in the mixture of odd-numbered carbon fatty acid triglycerides, DHA algae oil and high oleic sunflower oil, the weight ratio of pentadecanoic acid triglycerides 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 1 2-25%, 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%; or 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 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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