Substances and methods for improving intestinal health and homeostasis, as well as nutrition and development of subjects.

Abstract

The present invention provides a substance and method for improving intestinal health and homeostasis, as well as nutrition and development of subjects. The substance is an odd-carbon fatty acid. Specifically, the present invention provides the following uses of an odd-carbon fatty acid in the preparation of a formulation or pharmaceutical: increasing the protein expression of tight junction-related proteins of subjects; reducing the content of corticotropin-releasing hormone in the intestinal tissue of subjects; improving or strengthening the mechanical barrier of the intestinal tract of subjects; maintaining immune homeostasis in the intestinal tract of subjects; promoting the development of the intestinal tract of subjects and maintaining energy homeostasis of intestinal cells of subjects; and improving energy metabolism in the intestinal tract; promoting the development and metabolism of muscle tissue of subjects; promoting the development and metabolism of adipose tissue of subjects; reducing allergic reactions in the body and intestinal tract of subjects; reducing insulin resistance in pregnant subjects; controlling blood glucose levels in pregnant subjects; preventing gestational diabetes; preventing or improving gestational intrahepatic cholestasis in subjects; and preventing or treating diseases caused by Helicobacter pylori bacteria in subjects.

Description

Technical Field

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[0001] The present invention relates to substances and methods for improving intestinal health and homeostasis, as well as the nutrition and development of a subject.

Background Art

[0002] Odd-carbon fatty acids (OCFA) are a type of fatty acid having an odd number of carbon atoms. A small amount of OCFA is contained in natural lipids, which is a normal component of an animal body and is normally metabolized in the body. In the prior art, it is generally considered that the accumulation of OCFA in the human body does not affect the normal growth and development of the human body.

[0003] Some studies have shown that odd-carbon fatty acids have different properties and physiological effects from even-carbon fatty acids: odd-carbon fatty acids have a looser crystal structure and weaker intermolecular forces compared to even-carbon fatty acids; odd-carbon fatty acids have a different metabolic pathway in the human body from even-carbon fatty acids, and propionyl CoA produced by β-oxidation has a glycogen effect and is a dynamic endogenous indicator for the dietary evaluation of the human body; pentadecanoic acid and heptadecanoic acid can be used to evaluate the risk of coronary artery disease and diabetes; also, pentadecanoic acid and nonadecanoic acid have a strong inhibitory effect on the proliferation of various cancer cells.

Summary of the Invention

Problems to be Solved by the Invention

[0004] An object of the present invention is to develop a novel use of odd-carbon fatty acids or triglycerides containing odd-carbon fatty acids.

[0005] In particular, the present invention relates to any one, two, three, four, five, six, seven, eight, nine, ten, eleven, twelve, thirteen, fourteen, fifteen, sixteen, seventeen, eighteen, nineteen, twenty, or twenty-one of the 39 objectives described herein. The present invention provides the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for any purpose, whether 1, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, or 39.

[0006] The present invention further provides oils and fats for use in the above-mentioned applications. [Means for solving the problem]

[0007] The details of this invention are as follows: [Brief explanation of the drawing]

[0008] [Figure 1] Differences in the expression levels of various tight junction-related proteins in the duodenum, jejunum, and ileum of piglets that ingested different lipid supplements. [Figure 2] Differences in CRF content in the ileum of piglets that ingested different fat supplements. [Figure 3] Differences in IgG, IgA, and IgM content in the jejunum of piglets that ingested different fat supplements. [Figure 4] Differences in IgG, IgA, and IgM content in the ileum of piglets that ingested different fat supplements. [Figure 5] Differences in TLR4 and NF-κB protein expression levels in the duodenum, jejunum, and ileum of piglets ingesting different lipid supplements. [Figure 6]Differences in TNF-α, IL-1β, IL-6, and IL-10 content in the ileum of piglets that ingested different lipid supplements. [Figure 7] Differences in MUC-2 gene expression levels in the ileum of piglets that ingested different lipid supplements. [Figure 8] Differences in Ki67 protein expression levels in the duodenum, jejunum, and ileum of piglets that ingested different fat supplements. [Figure 9] Differences in p-mTOR (phosphorylated mTOR) protein expression levels in the duodenum, jejunum, and ileum of piglets that ingested different fat supplements. [Figure 10] Differences in p-p70S6K (phosphorylated p70S6K) protein expression levels in the duodenum, jejunum, and ileum of piglets that ingested different fat supplements. [Figure 11] Differences in the content of maltase in the duodenum and aminopeptidase N and sucrase in the ileum of piglets that ingested different fat supplements. [Figure 12] Differences in serotonin (5-hydroxytryptamine) content in the duodenum, jejunum, and ileum, and differences in SP content in the ileum, in piglets that ingested different fat supplements. [Figure 13] Differences in protein expression levels of major mitochondrial autophagy proteins ULK1, TFEB, and parkin in the duodenum and jejunum, as well as differences in protein expression levels of ULK1 and TFEB in the ileum, in piglets ingesting different lipid supplements. [Figure 14] Differences in PPARγ and SREBP-1 protein expression levels in the duodenum and jejunum of piglets ingesting different lipid supplements. [Figure 15] Differences in the protein expression levels of MYHC1, MYHC2a, MYHC2b, MYHC2x, mTOR, p-AMPK, and PGC1-α in the back muscles of piglets that ingested different lipid supplements. [Figure 16] Differences in SREBP-1C gene expression levels in the back muscles of piglets that consumed different fat supplements. [Figure 17] Differences in the protein expression levels of p-mTOR (phosphorylated mTOR), Prdm16, Irisin in the longissimus dorsi muscle of piglets fed different oil supplements, and p-mTOR and Prdm16 in the perirenal fat. [Figure 18] Differences in the gene expression levels of SREBP-1C and APOB in the longissimus dorsi muscle of piglets fed different oil supplements. [Figure 19] Differences in the levels of glutathione peroxidase (GSH-PX) content in the serum of piglets fed different oil supplements. [Figure 20] Differences in the contents of IgE and HIS in the serum, jejunum, and ileum of piglets fed different oil supplements. [Figure 21] Average daily gain, average daily feed intake, and feed conversion ratio of piglets fed different oil supplements during the experimental period (the average daily feed intake and feed conversion ratio of the breast milk group G0 could not be accurately statistically analyzed). [Figure 22] Ratio of the weight of the liver, brain, cerebellum, or brainstem to body weight of piglets fed different oil supplements. [Figure 23] Contents of serum cortisol and adrenocorticotropic hormone ACTH in piglets fed different oil supplements. [Figure 24] Contents of serum HDL-C, LDL-C, ALT, AST, TG, and CHOL in piglets fed different oil supplements. [Figure 25] Contents of serum TP, ALB, BUN, and CREA in piglets fed different oil supplements. [Figure 26] Content of serum TNF-α in piglets fed different oil supplements. [Figure 27] Contents of serum IgG, IgM, and splenic IgA in piglets fed different oil supplements. [Figure 28] Content of serum D-LACT in piglets fed different oil supplements. <000Fasting serum glucose (GLU), fasting serum insulin (INS) content levels, and fasting insulin resistance index in pregnant mice fed different oils and feed per day. [Figure 30] Serum bile acid content in pregnant mice fed different oils and feed per day. [Figure 31] Content levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and malondialdehyde (MDA) in the livers of pregnant mice fed different oils and feed per day. [Figure 32] Histological lesion scores and HE staining images of the large intestine in pregnant mice fed different oils and feed per day. [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 feed per day. [Figure 34] Ratio levels of determined sequences of Helicobacter pylori and Defluviibacter in the intestinal tracts of pregnant mice fed different oils and feed per day. [Figure 35] Feed conversion rate of pregnant mice fed different oils and feed per day during the experimental period. [Figure 36] Serum TC, TG, HDL, and LDL contents in pregnant mice fed different oils and feed per day. [Figure 37] Differences in HIF-1α protein expression levels in the duodenum, jejunum, and ileum of piglets fed different oil supplements. [Figure 38] Scanning electron microscope images of the intestinal tracts of piglets fed different oil supplements. [Figure 39] HE staining images of the intestinal tracts of piglets fed different oil supplements. [Figure 40] Duodenal villus height, duodenal crypt depth, and their ratio in piglets fed different oil supplements. [Figure 41]Jejunal villi height, jejunal crypt depth, and their ratio in piglets ingested different fat supplements. [Figure 42] Ileal villi height, ileal crypt depth, and their ratio in piglets ingesting different fat supplements. [Modes for carrying out the invention]

[0009] In the figure above, * indicates P<0.05, ** indicates P<0.01, *** indicates P<0.005, and ns indicates no significant difference.

[0010] Within the scope of the present invention, it should be understood that the technical features specified above and the technical features specifically described below (e.g., examples) can be combined to form preferred technical solutions. Unless otherwise specified, terms used herein have the same meaning as those generally understood by those skilled in the art. Unless otherwise specified, the various contents (X%) and ratios between components used in this application are based on weight ratios.

[0011] This application describes research on the physiological and medical effects of odd-carbon fatty acids, revealing novel biological activities and functions of these fatty acids. Therefore, this application aims to provide new applications for odd-carbon fatty acids.

[0012] In this specification, "odd-carbon fatty acid" refers to a fatty acid having an odd number of carbon atoms, and includes, but is 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-carbon fatty acids described in this application particularly include one or more 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 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).

[0013] In some embodiments, in the uses described herein, the C15:0 fatty acid content is 80% or more, preferably 85% or more, 90% or more, or 95% or more, based on the total amount of odd-carbon fatty acids. In some embodiments, the C15:0 fatty acid content is 99% or more, based on the total amount of odd-carbon fatty acids. In some embodiments, in the uses described herein, the odd-carbon fatty acids further include C17:0 in addition to C15:0, and based on the total weight of odd-carbon fatty acids, the C17:0 content is ≤18%; in some embodiments, the C17:0 content is ≤13%; in some embodiments, the C17:0 content is ≤5%; in some embodiments, the C17:0 content is ≤3%; in some embodiments, the C17:0 content is ≤1%.

[0014] In the use of odd-carbon fatty acids as described herein, it should be understood that odd-carbon fatty acids may be used in the form of odd-carbon fatty acids themselves, or in the form of fatty acid chains contained in glycers such as monoglycerides, diglycerides, and / or triglycerides. In some embodiments, triglycerides are fats and oils. In this specification, the content of a particular fatty acid based on the total amount of odd-carbon fatty acids has the following conventional meanings: (1) the ratio of the fatty acid to the total amount of odd-carbon fatty acids if it exists in the form of a fatty acid; and (2) the ratio of fatty acid residues to the total amount of fatty acid residues bound to the glyceride if it exists in the form of a glyceride. Unless otherwise specified, the content herein is expressed in weight or weight percentage.

[0015] Accordingly, in some embodiments, this application provides the use of glycerides such as oils and fats containing odd-carbon fatty acids in their fatty acid composition. Preferably, in the fatty acid composition of glycerides, particularly oils and fats, the content of odd-carbon fatty acids is ≥20%, for example, 20% to 70%, or 20% to 60%. The odd-carbon fatty acid composition of glycerides, particularly oils and fats, may contain any one of the above-mentioned odd-carbon fatty acids, preferably at least 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 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 glycerides, especially the odd-carbon fatty acids of the oils and fats, include at least a C15:0 fatty acid (pentadecanoic acid).

[0016] In the odd-carbon fatty acid composition of glycerides, particularly oils and fats, the C15:0 fatty acid content is 80% or more, preferably 85% or more, 90% or more, or 95% or more, relative to the total amount of odd-carbon fatty acids. In some embodiments, the C15:0 fatty acid content is 99% or more based on the total amount of odd-carbon fatty acids. In some embodiments, the odd-carbon fatty acids further include C17:0 in addition to C15:0; the C17:0 content is ≤18% based on the total weight of odd-carbon fatty acids; in some embodiments, the C17:0 content is ≤13%; in some embodiments, the C17:0 content is ≤5%; in some embodiments, the C17:0 content is ≤3%; in some embodiments, the C17:0 content is ≤1%.

[0017] In some embodiments, the fatty acid content of glycerides, particularly oils and fats, is 5% or less, preferably 1% or less, and more preferably 0.5% or less; The C13:0 fatty acid content is 1% to 5%, preferably 2% to 4%; the C15:0 fatty acid content is 15% to 70%, preferably 18% to 60%; the C17:0 fatty acid content is 0.1% to 9%; the C19:0 fatty acid content is 5% or less, preferably 1% or less, more preferably 0.5% or less; the C21:0 fatty acid content is 5% or less, preferably 1% or less, more preferably 0.5% or less; and the C23:0 fatty acid content is 5% or less, preferably 1% or less, even more preferably 0.5% or less.

[0018] In some embodiments, the fatty acid composition of glycerides, particularly oils and fats, further includes one or more of the following: 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 glycerides, particularly oils and fats, the C16:0 content may be 2% to 15%, for example 4% to 13%; the C18:0 content may be ≤5%, for example 0% to 5% or 0% to 3%; the C18:1 content may be 5% to 35%, for example 7% to 33%; the C18:2 content may be ≤35%, for example 0% to 35%; the C22:5 content may be ≤5%, for example 0% to 5% or 1% to 3.5%; the C22:6 content may be 5% to 25%, for example 8% to 22%; and the content of the remaining fatty acids is usually 1% or less or less than 0.5%.

[0019] In some embodiments, the fatty acid composition of glycerides, particularly oils and fats, is such that the C13:0 content is 1% to 5%, preferably 2% to 4%, the C15:0 content is 40% to 60%, preferably 45% to 53%, the C16:0 content is 1% to 7%, preferably 3% to 5.5%, the C17:0 content is 4% to 9%, preferably 5% to 9%, the C18:1 content is 5% to 10%, preferably 6% to 8%, the C22:5 content is 1% to 5%, preferably 2% to 4%, and the C22:6 content is 15% to 25%, preferably 18% to 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 glycerides, particularly oils and fats, is such that the C15:0 content is 40% to 65%, preferably 50% to 60%, the C16:0 content is 1% to 7%, preferably 3% to 5.5%, the C17:0 content is 0.1% to 3%, preferably 0.1% to 1%, the C18:0 content is 1% to 5%, preferably 1% to 3%, the C18:1 content is 25% to 35%, preferably 28% to 34%, and the C18:2 content is 1% to 5%, preferably 2% to 4%; the content of the remaining fatty acids is usually less than 1% or less than 0.5%.

[0020] In some embodiments, the fatty acid composition of glycerides, particularly oils and fats, is such that the C15:0 content is 12% to 25%, preferably 16% to 22%, the C16:0 content is 5% to 15%, preferably 10% to 15%, the C17:0 content is 1% to 7%, preferably 2% to 5%, the C18:0 content is 0.5% to 3%, preferably 1% to 2%, the C18:1 content is 12% to 22%, preferably 15% to 20%, the C18:2 content is 25% to 35%, preferably 30% to 35%, and the C22:6 content is 5% to 15%, preferably 7% to 12%; the content of the remaining fatty acids is usually less than 1% or less than 0.5%.

[0021] Please note that the content of each fatty acid in the fatty acid composition described herein is measured by referring to the third method, i.e., the "normalization method," in "GB5009.168-2016 Food Safety National Standard Determination of Fatty Acids in Foods."

[0022] In some embodiments, the fats and oils are derived from edible oils (e.g., one or more edible oils), transesterification products of edible oils, or any combination thereof. In some embodiments, triglycerides containing odd-carbon fatty acids are prepared by transesterification with conventional edible oils.

[0023] In some embodiments, the edible oil is selected from vegetable oils, microbial oils, animal oils, or any combination thereof, and preferably the vegetable oil includes one or more of the following: rice bran 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, Triadica cevifera seed oil, sweet almond oil, almond oil, Vernicia fuciformis Walnut 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, cocoa butter, or fractions thereof, their auto-transesterification products, or transesterification products of two or more fats and oils; animal oils are selected from one or more of lard, chicken fat, mutton fat, fish oil, and beef tallow.

[0024] In some embodiments, the microorganism is selected from algae, e.g., the order Traustochytriales (which more specifically includes strains of the genera Traustochytrium and Schizochytrium); oily bacteria, e.g., the genus Rhodococcus (e.g., Rhodococcus opacus); oily yeasts, e.g., the genus Yarowia (e.g., Yarowia liporitica); and mutant strains and mixed strains derived from any of the above strains, with the microorganism preferably being of the genus Schizochytrium.

[0025] Transesterification includes chemical transesterification and enzymatic transesterification. Chemical transesterification can be carried out using chemical catalysts conventionally used in chemical transesterification. Exemplary chemical catalysts include, but are not limited to, acidic and basic catalysts. Preferably, the chemical catalyst is NaOH, KOH, NaOCH3, sodium ethoxide, organic base, solid base catalyst, sulfuric acid, sulfonic acid, or solid acid catalyst; more preferably, the chemical catalyst is NaOH, KOH, NaOCH3, sulfuric acid, or sulfonic acid; and even more preferably, the chemical catalyst is sodium methoxide, NaOH, and / or KOH. The amount of chemical catalyst used may be 0.1% to 1.0% of the total weight of the raw material oil. The chemical catalyst can be used in forms well known in the art. For example, sodium methoxide is usually added to the raw material oil in solid form, and NaOH and KOH are usually used in aqueous solution form. The concentration of the aqueous solution can be, for example, 30% to 50%. The amounts used described herein are the amounts of the catalyst itself, not the amounts of the solution. The reaction can be carried out at a temperature of 80°C to 150°C, preferably 100°C to 120°C. The reaction can be carried out under reduced pressure (e.g., vacuum degree ≤ 10 mbar) for a certain period of time (e.g., 0.5 hours to 1 hour) so that the fatty acids are uniformly distributed on the glycerol backbone. After the transesterification is complete, the reaction product is washed with water.

[0026] When using enzymatic transesterification, lipase can be used as a catalyst. Lipase can be lipase powder or immobilized lipase, where lipase is immobilized on a carrier (e.g., diatomaceous earth, ion exchange resin, etc.). Preferably, a lipase lacking site specificity is used, such as lipase derived from the genus Alcaligenes or Candida, but not limited to these. Suitable lipases include various commercially available immobilized enzymes or their fermentation solutions. For example, Novozymes' Lipozyme TL IM, Lopozyme RM, etc., and immobilized enzymes or their fermentation solutions from Amano Enzyme Co., Ltd. of Japan. The amount of lipase added is usually 1 / 10,000 to 1 / 100,000 of the weight of the raw oil. The pre-transesterification reaction temperature can be in the range of 40°C to 80°C, for example, 70±5°C, depending on the optimal reaction temperature of the lipase used. Similarly, the pre-transesterification treatment is stopped when the transesterification rate reaches 0.1% to 1.0%. The reaction time for the enzymatic pre-transesterification treatment can range from 0.5 hours to 10 hours, for example, from 0.5 hours to 3 hours, depending on the specific reaction conditions.

[0027] After the transesterification process is complete, the resulting transesterified oil can be subjected to conventional refining processes such as decolorization and deodorization.

[0028] Glycerides containing odd-carbon fatty acids can be produced by reacting odd-carbon fatty acids with glycerol. For example, odd-carbon fatty acids and glycerol can undergo esterification in the presence of lipase. Suitable lipases include the immobilized enzyme NOVO435 (Novozymes), which are commonly used in esterification reactions in this art. Generally, the molar ratio of odd-carbon fatty acids to glycerol is 2 to 5:1. The odd-carbon fatty acids used in the esterification reaction may be a mixture of several types of odd-carbon fatty acids or a single type of odd-carbon fatty acid. Generally, after mixing odd-carbon fatty acids and glycerol, the mixture is heated to 65°C to 75°C, and then lipase is added in an amount of 1% to 20% of the substrate weight, for example, 5% to 15%, and the reaction is carried out under a vacuum of ≤10 mbar until the reaction is complete, thereby obtaining glycerides containing odd-carbon fatty acids used in this invention. The reaction can be carried out under stirring conditions. The resulting glycerides containing odd-carbon fatty acids can be purified by molecular distillation.

[0029] The edible oils used in transesterification may be vegetable oils, microbial oils, or animal oils well known in the art, including but not limited to the following: rice bran 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, Triadica cevifera seed oil, sweet almond oil, almond oil, Vernicia fordii seed oil, rubber seed oil, corn oil, wheat germ oil, sesame oil, castor seed oil, evening primrose seed oil, hazelnut oil, pumpkin seed oil, walnut oil, grape seed oil, borage seed oil, sea buckthorn seed oil, tomato seed oil, macadamia nut oil, coconut oil, and cocoa butter—one or more of these. The animal oils are selected from one or more of lard, chicken fat, mutton fat, fish oil, and beef tallow. Microbial oils include algal oils. Edible oils also include transesterification and fractional distillation products of various oils, including, but not limited to, various stearins obtained by fractional distillation, such as palm stearin. Depending on other effects that are desired, an appropriate edible oil may be selected. For example, algal oils rich in DHA (docosahexaenoic acid) and / or vegetable oils rich in oleic acid (such as high-oleic sunflower seed oil) can be selected. In some embodiments, the edible oil may further contain palm stearin.

[0030] When performing transesterification, an appropriate ratio of triglycerides containing odd-carbon fatty acids to vegetable oil can be selected depending on the specific reaction conditions and the desired odd-carbon fatty acid content in the oil. For example, in some embodiments, the weight ratio of triglycerides containing odd-carbon fatty acids to vegetable oil may be 45-70:30-55. In some embodiments, the weight ratio of triglycerides containing odd-carbon fatty acids to vegetable oil may be 50-65:35-50. In some embodiments, the weight ratio of triglycerides containing odd-carbon fatty acids to vegetable oil may be 55-62:38-45.

[0031] In some embodiments, the oil is a chemical transesterification product of an odd-carbon fatty acid-containing triglyceride with DHA algae oil and high-oleic sunflower seed oil; preferably, in a mixture of an odd-carbon fatty acid-containing triglyceride with DHA algae oil and high-oleic sunflower seed oil, the weight ratio of triglyceride pentadecanoic acid, DHA algae oil, and high-oleic sunflower seed oil is 40-50:30-45:1-10, for example, 40-50:30-40:5-10 or 40-50:38-45:1-5. In some embodiments, the fatty acid composition of the oil and fat is such that the C15:0 content is 12% to 25%, preferably 16% to 22%, the C16:0 content is 5% to 15%, preferably 10% to 15%, the C17:0 content is 1% to 7%, preferably 2% to 5%, the C18:0 content is 0.5% to 3%, preferably 1% to 2%, the C18:1 content is 12% to 22%, preferably 15% to 20%, the C18:2 content is 25% to 35%, preferably 30% to 35%, and the C22:6 content is 5% to 15%, preferably 7% to 12%; the content of the remaining fatty acids is usually less than 1% or less than 0.5%.

[0032] In some embodiments, the fat is a chemical transesterification product of an odd-carbon fatty acid-containing triglyceride, palm stearin, and high-oleic sunflower seed oil; preferably, in a mixture of an odd-carbon fatty acid-containing triglyceride, palm stearin, and high-oleic sunflower seed oil, the weight ratio of pentadecanoic acid triglyceride to palm stearin and high-oleic sunflower seed oil is 55-62:1-5:35-40. In some embodiments, the fatty acid composition of the oil and fat is such that the C15:0 content is 40% to 65%, preferably 50% to 60%, the C16:0 content is 1% to 7%, preferably 3% to 5.5%, the C17:0 content is 0.1% to 3%, preferably 0.1% to 1%, the C18:0 content is 1% to 5%, preferably 1% to 3%, the C18:1 content is 25% to 35%, preferably 28% to 34%, and the C18:2 content is 1% to 5%, preferably 2% to 4%; the content of the remaining fatty acids is usually less than 1% or less than 0.5%.

[0033] The uses of odd-carbon fatty acids described herein include one or more of the following odd-carbon fatty acids, and also include the use of odd-carbon fatty acids in the manufacture of formulations or pharmaceuticals for one or more of the following purposes: (1) Increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in the target; in particular, increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in the intestinal tract (e.g., intestinal mucosa), more specifically, increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in the duodenum, jejunum, and ileum (e.g., their mucosa); (2) To reduce the amount of corticotropin-releasing hormone (CRF) in the target intestinal tissue; more preferably, to reduce the amount of corticotropin-releasing hormone (CRF) in the ileal tissue; (3) To improve or strengthen the mechanical barrier of the target intestinal tract; by improving the mechanical barrier of the intestinal tract, it is possible to prevent the invasion of bacteria, toxins, and foreign antigens into the body, maintain the stability of the internal environment, and prepare the foundation for nutrient absorption; (4) Increasing the content of immunoglobulins (e.g., IgG, IgA, and / or IgM) in the target intestinal tract; preferably increasing the content of immunoglobulins (e.g., 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; even more preferably increasing the content of immunoglobulin A in the ileum; (5) To increase the protein expression levels of TLR4 and NF-κB in the target intestinal tissue, particularly in the duodenum, jejunum, and ileum; (6) Maintaining homeostasis of ileal inflammatory cytokines (e.g., TNF-α, IL-1β, IL-6, and / or IL-10) in the subject; (7) To increase the expression level of ileal mucin 2 in the subjects; (8) To increase the expression of HIF-1α in the intestinal tract and promote the survival of intestinal cells in a hypoxic environment within the intestinal tract; (9) Maintaining immune homeostasis in the target intestinal tract (especially the ileum); (10) To increase the content of the nuclear protein Ki-67 in the target intestinal tissue and promote the proliferation of the target intestinal epithelial cells, the intestinal tissue is preferably the duodenum, jejunum and / or ileum; (11) Activating the mTOR signaling pathway in the target intestinal tract, increasing the expression level of activated mTOR protein in intestinal cells (particularly small intestinal cells such as the duodenum, jejunum, and ileum), and / or increasing the level of activated S6 kinase in intestinal cells (particularly small intestinal cells such as the duodenum, jejunum, and ileum); (12) To increase the levels of digestive enzymes (including but not limited to maltase, aminopeptidase and / or sucrase) in the target intestinal tract, particularly the small intestine, and to promote the absorption of nutrients; (13) To increase the 5-hydroxytryptamine content in the target intestinal tissue (especially the duodenum, jejunum, and / or ileum) and the substance P (neuropeptide) content in the ileum, thereby enhancing the function of the small intestine, such as by increasing intestinal peristalsis, promoting the contraction of gastrointestinal smooth muscle, suppressing the secretion of gastric acid and bile, and regulating local gastrointestinal blood flow; (14) To promote the development of the target intestinal tract; (15) Downregulating the expression levels of mitochondrial autophagy-related proteins (e.g., ULK1, TFEB, and / or parkin) in cells of the target intestinal tract (particularly the duodenum, jejunum, and / or ileum) to alleviate mitochondrial dysfunction; (16) Upregulating the levels of lipid synthesis-related transcription factors (such as PPARγ and / or SREBP-1) in the target intestinal tract (especially the small intestine, especially the duodenum and jejunum) to promote lipid absorption and assimilation in the intestinal tract (especially the small intestine, especially the duodenum and jejunum); (17) To maintain energy homeostasis of target intestinal cells and improve energy metabolism in the intestines; (18) Upregulating the content of type I and type II muscle fibers and the expression level of mTOR protein in the target muscle tissue, while simultaneously decreasing the relative content of AMPK and PGC1-α; (19) To improve the energy state of the target 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; (20) To upregulate the expression level of SREBP-1 in target muscle tissue, promote lipid anabolism, increase lipid uptake and utilization by muscle tissue, improve energy status, and promote muscle tissue development and metabolism; (21) To promote the development and metabolism of the target muscle tissue; (22) Upregulating the expression of activated mTOR in the target, decreasing the expression levels of Prdm16 and Irisin, inhibiting lipolysis, increasing lipid synthesis, and promoting the development of adipose tissue; (23) To upregulate the levels of SERBP-1 and APOB in the target adipose tissue, increase lipid synthesis in adipose tissue, promote lipid transport in the body, and maintain the energy balance between adipose tissue and the body; (24) To promote the development and metabolism of the target adipose tissue; (25) To upregulate the GSH-PX content in the target serum, improve the body's overall antioxidant capacity, and maintain overall redox equilibrium; (26) To reduce the levels of HIS, jejunal IgE, ileal IgE, jejunal HIS, and ileal HIS in the target blood, thereby reducing allergic reactions in the body and in the jejunum and ileum; (27) To reduce allergic reactions in the body and intestinal tract of the subject; (28) To reduce insulin resistance in pregnant subjects; (29) Controlling blood glucose levels in pregnant subjects; (30) To improve insulin resistance caused by an unhealthy diet (e.g., a low-protein diet); (31) To prevent gestational diabetes, and to prevent macrosomia, fetal malformations, premature birth, premature membrane rupture and / or polyhydramnios caused by gestational diabetes, and to reduce fetal mortality; (32) To lower serum bile acid levels in pregnant subjects; (33) To prevent or improve pregnancy-related intrahepatic cholestasis (e.g., pregnancy-related intrahepatic cholestasis caused by inappropriate diet or disease) in the subjects; and to reduce the occurrence or risk of occurrence of fetal distress, premature birth, and perinatal mortality associated with pregnancy-related intrahepatic cholestasis in the subjects; (34) To increase the levels of superoxide dismutase and glutathione peroxidase in the liver of the subject, and to decrease the level of malondialdehyde in the liver of the subject, thereby reducing oxidative stress in the pregnant subject; (35) To improve the pathological damage to intestinal tissue caused by the abnormal diet or disease of the subject; (36) To reduce inflammatory bowel factors (e.g., IL-1β, IL-6, TNF-α, NLRP3, and / or GSDMD) in the subject and reduce inflammation of the intestinal tract; (37) To treat or prevent inflammatory bowel disease and colorectal cancer; (38) To reduce the amount of Helicobacter pylori and / or Deferibacter species in the subject's body and improve the microbial ecosystem in the intestinal tract; and (39) To prevent or treat diseases, including gastric cancer, caused by Helicobacter pylori bacteria in the target population.

[0034] In some embodiments, the use of odd-carbon fatty acids described herein includes the following uses of odd-carbon fatty acids, and also includes the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for the following purposes: (1) Increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in the subject; in particular, increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in the intestinal tract (e.g., intestinal mucosa), more specifically, increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in the duodenum, jejunum, and ileum (e.g., their mucosa); and (2) To reduce the amount of corticotropin-releasing hormone (CRF) in the target intestinal tissue; This improves or strengthens the mechanical barrier of the target intestinal tract.

[0035] In some embodiments, the use of odd-carbon fatty acids described herein includes the following uses of odd-carbon fatty acids, and also includes the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for one or more of the following purposes: (4) Increasing the content of immunoglobulins (e.g., IgG, IgA, and / or IgM) in the target intestinal tract; preferably increasing the content of immunoglobulins (e.g., 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; even more preferably increasing the content of immunoglobulin A in the ileum; (5) To increase the protein expression levels of TLR4 and NF-κB in the target intestinal tissue, particularly in the duodenum, jejunum, and ileum; (6) Maintaining homeostasis of ileal inflammatory cytokines (e.g., TNF-α, IL-1β, IL-6, and / or IL-10) in the subject; (7) To increase the expression level of ileal mucin 2 in the subjects; (8) To increase the expression of HIF-1α in the intestinal tract and promote the survival of intestinal cells in a hypoxic environment within the intestinal tract; (9) To maintain immune homeostasis in the target intestinal tract (especially the ileum).

[0036] In some embodiments, the use of odd-carbon fatty acids described herein includes the following uses of odd-carbon fatty acids, and also includes the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for one or more of the following purposes: (10) To increase the content of the nuclear protein Ki-67 in the target intestinal tissue and promote the proliferation of the target intestinal epithelial cells, the intestinal tissue is preferably the duodenum, jejunum and / or ileum; (11) Activating the mTOR signaling pathway in the target intestinal tract, increasing the expression level of activated mTOR protein in intestinal cells (particularly small intestinal cells), and / or increasing the level of activated S6 kinase in intestinal cells (particularly small intestinal cells); (12) To increase the levels of digestive enzymes (including but not limited to maltase, aminopeptidase and / or sucrase) in the target intestinal tract, particularly the small intestine, and to promote the absorption of nutrients; and (13) To increase the 5-hydroxytryptamine content in the target intestinal tissue (especially the duodenum, jejunum, and / or ileum) and the substance P content in the ileum, thereby enhancing the function of the small intestine, such as by increasing intestinal peristalsis, promoting the contraction of gastrointestinal smooth muscle, suppressing the secretion of gastric acid and bile, and regulating local gastrointestinal blood flow; This promotes the development of the target intestinal tract.

[0037] In some embodiments, the use of odd-carbon fatty acids described herein includes the following uses of odd-carbon fatty acids, and also includes the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for one or more of the following purposes: (15) Downregulating the expression levels of mitochondrial autophagy-related proteins (e.g., ULK1, TFEB, and / or parkin) in target intestinal cells to alleviate mitochondrial dysfunction; and / or (16) Upregulating the levels of lipid synthesis-related transcription factors (such as PPARγ and / or SREBP-1) in the target intestinal tract (especially the small intestine) to promote lipid absorption and assimilation in the intestinal tract (especially the small intestine, especially the duodenum and jejunum); This maintains the energy homeostasis of the target intestinal cells and improves energy metabolism in the intestines.

[0038] In some embodiments, the use of odd-carbon fatty acids described herein includes the following uses of odd-carbon fatty acids, and also includes the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for one or more of the following purposes: (18) Upregulating the content of type I and type II muscle fibers and the expression level of mTOR protein in the target muscle tissue, while simultaneously decreasing the relative content of AMPK and PGC1-α; and / or (19) To improve the energy state of the target 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; and / or (20) To upregulate the expression level of SREBP-1 in target muscle tissue, promote lipid anabolism, increase lipid uptake and utilization by muscle tissue, improve energy status, and promote muscle tissue development and metabolism; This promotes the development and metabolism of the target muscle tissue.

[0039] In some embodiments, the use of odd-carbon fatty acids described herein includes the following uses of odd-carbon fatty acids, and also includes the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for one or more of the following purposes: (22) Upregulating the expression of activated mTOR in the subject, decreasing the expression levels of Prdm16 and Irisin, inhibiting lipolysis, increasing lipid synthesis, and promoting the development of adipose tissue; and / or (23) To upregulate the levels of SERBP-1 and APOB in the target adipose tissue, increase lipid synthesis in adipose tissue, promote lipid transport in the body, and maintain the energy balance between adipose tissue and the body; This promotes the development and metabolism of the target adipose tissue.

[0040] In some embodiments, the use of odd-carbon fatty acids described herein includes the following uses of odd-carbon fatty acids, and also includes the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for one or more of the following purposes: (25) Upregulating the GSH-PX content in the serum of the subject, improving the body's overall antioxidant capacity, and maintaining overall redox equilibrium; and / or (26) To reduce the levels of HIS, jejunal IgE, ileal IgE, jejunal HIS, and ileal HIS in the target blood, thereby reducing allergic reactions in the body and in the jejunum and ileum; This reduces allergic reactions in the target body and intestinal tract.

[0041] In some embodiments, the use of odd-carbon fatty acids described herein includes the following uses of odd-carbon fatty acids, and also includes the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for one or more of the following purposes: (28) To reduce insulin resistance in pregnant subjects; and / or (29) Controlling blood glucose levels in pregnant subjects; This prevents gestational diabetes, and prevents macrosomia, fetal malformations, premature birth, premature membrane rupture and / or polyhydramnios caused by gestational diabetes, thereby reducing fetal mortality.

[0042] In some embodiments, the uses of odd-carbon fatty acids described herein include the following uses of odd-carbon fatty acids, and also the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for the following purposes: to lower serum bile acid levels in pregnant subjects, thereby preventing or improving pregnancy-related intrahepatic cholestasis (e.g., pregnancy-related intrahepatic cholestasis caused by an inappropriate diet or disease) in subjects. In some embodiments, the uses of odd-carbon fatty acids described herein include the following uses of odd-carbon fatty acids, and also the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for the following purposes: to reduce the occurrence or risk of occurrence of fetal distress, premature birth, and perinatal mortality associated with pregnancy-related intrahepatic cholestasis in subjects.

[0043] In some embodiments, the uses of odd-carbon fatty acids described herein include the following uses of odd-carbon fatty acids, and also the uses of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for the following purposes: to improve the pathological damage effect on intestinal tissue caused by an abnormal diet or disease of a subject by increasing the levels of superoxide dismutase and glutathione peroxidase in the liver of a subject, decreasing the levels of malondialdehyde in the liver of a subject, and reducing oxidative stress in a pregnant subject.

[0044] In some embodiments, the use of odd-carbon fatty acids as described herein includes the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for the following purposes: to reduce inflammatory factors in the colon in a subject, thereby treating or preventing inflammatory bowel disease and colorectal cancer.

[0045] In some embodiments, the use of odd-carbon fatty acids described herein includes the following uses of odd-carbon fatty acids, and also the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for the following purposes: to reduce Helicobacter pylori in the body of a subject, thereby preventing or treating diseases caused by Helicobacter pylori bacteria, including gastric cancer of a subject.

[0046] In some embodiments, the use of odd-carbon fatty acids described herein includes the following uses of odd-carbon fatty acids, and also includes the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for the following purposes: To improve or strengthen the mechanical barrier of the target intestinal tract, maintain immune homeostasis in the target intestinal tract (especially the ileum), promote the development of the target intestinal tract, maintain energy homeostasis of cells in the target intestinal tract, and improve energy metabolism in the intestinal tract; and / or To promote the development and metabolism of the target muscle tissue; and / or To promote the development and metabolism of the target adipose tissue; and / or To reduce allergic reactions in the body and intestinal tract of the target individual.

[0047] In some embodiments, the use of odd-carbon fatty acids described herein includes the following uses of odd-carbon fatty acids, and also includes the use of odd-carbon fatty acids in the preparation of formulations or pharmaceuticals for the following purposes: To improve the level of intestinal health, which preferably involves strengthening the mechanical barrier function of the intestines, enhancing immune homeostasis in the intestines, promoting intestinal development, increasing digestive enzyme levels in the intestines, enhancing nutrient absorption, maintaining energy homeostasis of intestinal cells, improving pathological damage to intestinal tissue, reducing inflammation in the intestines, and / or improving the microbial ecology in the intestines; and / or To improve the development and metabolism of muscle tissue; and / or To improve the development and metabolism of adipose tissue; and / or To improve antioxidant capacity or reduce oxidative stress; and / or To reduce allergic reactions, preferably in the intestinal tract; and / or Improving insulin resistance through a low-protein diet; and / or To improve bile acid metabolism.

[0048] In some embodiments, the use of odd-carbon fatty acids described herein includes the following uses of odd-carbon fatty acids, and also the use of odd-carbon fatty acids in the manufacture of prophylactic, therapeutic or adjunctive 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 bacterial abnormalities, Helicobacter pylori infection, gestational diabetes (especially in gestational diabetes patients who are on or accompanied by a low-protein diet), and intrahepatic cholestasis (especially gestational intrahepatic cholestasis).

[0049] In some embodiments, the following methods are also provided herein: (1) Methods for increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in a subject; in particular, methods for increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in the intestinal tract (e.g., intestinal mucosa), more specifically, methods for increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in the duodenum, jejunum, and ileum (e.g., their mucosa); (2) A method for reducing the amount of corticotropin-releasing hormone (CRF) in the target intestinal tissue; more preferably, a method for reducing the amount of corticotropin-releasing hormone (CRF) in the ileal tissue; (3) Methods for improving or strengthening the mechanical barrier of the target intestinal tract; (4) Methods for increasing the content of immunoglobulins (e.g., IgG, IgA, and / or IgM) in the target intestinal tract; preferably, methods for increasing the content of immunoglobulins (e.g., IgG, IgA, and / or IgM) in the jejunum and ileum; more preferably, methods for increasing the content of immunoglobulins IgG, IgA, and / or IgM in the jejunum; even more preferably, methods for increasing the content of immunoglobulin A in the ileum; (5) Methods for increasing the protein expression levels of TLR4 and NF-κB in target intestinal tissue, particularly in the duodenum, jejunum, and ileum; (6) Methods for maintaining homeostasis of ileal inflammatory cytokines (e.g., TNF-α, IL-1β, IL-6, and / or IL-10) in subjects; (7) Methods for increasing the expression level of ileal mucin 2 in the subject; (8) A method to increase the expression of HIF-1α in the intestinal tract and promote the survival of intestinal cells in a hypoxic environment in the intestinal tract; (9) Methods for maintaining immune homeostasis in the target intestinal tract (especially the ileum); (10) A method for increasing the content of nuclear protein Ki-67 in a target intestinal tissue, wherein the intestinal tissue is preferably the duodenum, jejunum and / or ileum, and a method for promoting the proliferation of target intestinal epithelial cells; (11) Methods for activating the mTOR signaling pathway in the target intestinal tract, and methods for increasing the expression level of activated mTOR protein in intestinal cells (particularly cells of the small intestine such as the duodenum, jejunum, and ileum), and / or increasing the level of activated S6 kinase in intestinal cells (particularly cells of the small intestine such as the duodenum, jejunum, and ileum); (12) Methods for increasing the levels of digestive enzymes (including but not limited to maltase, aminopeptidase and / or sucrase) in the target intestinal tract, particularly the small intestine, and thereby promoting the absorption of nutrients; (13) Methods for increasing the 5-hydroxytryptamine content in the tissues of the target intestinal tract (especially the duodenum, jejunum, and / or ileum) and the substance P (neuropeptide) content in the ileum, as well as methods for enhancing the function of the small intestine, such as increasing intestinal peristalsis, promoting the contraction of smooth muscle of the gastrointestinal tract, suppressing the secretion of gastric acid and bile, and regulating local gastrointestinal blood flow; (14) Methods to promote intestinal development in subjects; (15) A method for reducing mitochondrial dysfunction by downregulating the expression levels of mitochondrial autophagy-related proteins (e.g., ULK1, TFEB, and / or parkin) in cells of the target intestinal tract (particularly the duodenum, jejunum, and / or ileum); (16) A method for increasing the absorption and assimilation of intestinal lipids in the intestinal tract (particularly the small intestine, particularly the duodenum and jejunum) by upregulating the levels of lipid synthesis-related transcription factors (e.g., PPARγ and / or SREBP-1) in the target intestinal tract (particularly the small intestine, particularly the duodenum and jejunum); (17) Methods for maintaining energy homeostasis of target intestinal cells and improving energy metabolism in the intestines; (18) A method for upregulating the content of type I and type II muscle fibers and the expression level of mTOR protein in target muscle tissue, while simultaneously reducing the relative content of AMPK and PGC1-α; (19) A method for improving the energy state of target 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 overall muscle tissue development; (20) A method for upregulating the expression level of SREBP-1 in target muscle tissue, promoting lipid anabolism, increasing lipid uptake and utilization by muscle tissue, improving energy status, and promoting muscle tissue development and metabolism; (21) Methods for promoting the development and metabolism of target muscle tissue; (22) A method for promoting adipose tissue development by upregulating the expression of activated mTOR in a target, decreasing the expression levels of Prdm16 and Irisin, suppressing lipolysis, and increasing lipid synthesis; (23) A method for upregulating the levels of SERBP-1 and APOB in target adipose tissue, increasing lipid synthesis in adipose tissue, promoting lipid transport in the body, and maintaining the energy balance of adipose tissue and the body; (24) Methods for promoting the development and metabolism of adipose tissue in subjects; (25) Methods to upregulate the GSH-PX content in the target serum, improve the body's overall antioxidant capacity, and maintain overall redox equilibrium; (26) A method for reducing the levels of HIS, jejunal IgE, ileal IgE, jejunal HIS, and ileal HIS in the target blood, thereby reducing allergic reactions in the body and in the jejunum and ileum; (27) Methods for reducing allergic reactions in the body and intestinal tract of the subject; (28) Methods for reducing insulin resistance in pregnant subjects; (29) Methods for controlling blood glucose levels in pregnant women; (30) Methods to improve insulin resistance caused by an unhealthy diet (e.g., a low-protein diet); (31) Methods for preventing gestational diabetes, and methods for preventing macrosomia, fetal malformations, premature birth, premature membrane rupture and / or polyhydramnios caused by gestational diabetes, and for reducing fetal mortality; (32) Methods to lower serum bile acid levels in pregnant subjects; (33) Methods for preventing or improving pregnancy-related intrahepatic cholestasis in subjects, such as pregnancy-related intrahepatic cholestasis caused by inappropriate diet or disease; and methods for the occurrence or reduction of the risk of fetal distress, premature birth, and perinatal mortality in subjects with pregnancy-related intrahepatic cholestasis; (34) A method to increase the levels of superoxide dismutase N and glutathione peroxidase in the liver of a subject, decrease the level of malondialdehyde in the liver of a subject, and reduce oxidative stress in a pregnant subject; (35) Methods to improve the pathological damage effect on intestinal tissue caused by an abnormal diet or disease of the subject; (36) Methods for reducing inflammatory bowel factors (e.g., IL-1β, IL-6, TNF-α, NLRP3 and / or GSDMD) in subjects and reducing intestinal inflammation; (37) Methods for treating or preventing inflammatory bowel disease and colorectal cancer; (38) A method for reducing the amount of Helicobacter pylori and / or Deferibacter species in the body of a subject and improving the microbial ecosystem in the intestinal tract; and (39) Methods for preventing or treating diseases, including gastric cancer, caused by Helicobacter pylori bacteria in the subject.

[0050] Each method involves administering an effective amount of odd-carbon fatty acid to a subject requiring it. The odd-carbon fatty acid is as described in any embodiment herein. It should be understood that the odd-carbon fatty acid may be provided in the form of a free odd-carbon fatty acid, or in the form of a glyceride (such as a monoglyceride, diglyceride, and / or triglyceride) containing the odd-carbon fatty acid, or further in the form of a fat or oil (such as a fat or oil as described herein).

[0051] In some embodiments of the uses and methods described herein, the fats and oils have the following fatty acid composition: a C15:0 content of 50% to 60%, preferably 55% to 60%; a C16:0 content of 1% to 7%, preferably 3% to 5.5%; a C17:0 content of 0.1% to 3%, preferably 0.1% to 1%; a C18:0 content of 1% to 5%, preferably 1% to 3%; a C18:1 content of 25% to 35%, preferably 28% to 34%; and a C18:2 content of 1% to 5%, preferably 2% to 4%; the content of the remaining fatty acids is generally less than 1% or less than 0.5%. In some embodiments, the fat is a chemical transesterification product of a triglyceride containing odd-carbon fatty acids with palm stearin and high-oleic sunflower seed oil; preferably, in a mixture of a triglyceride containing odd-carbon fatty acids with palm stearin and high-oleic sunflower seed oil, the weight ratio of triglyceride pentadecanoate to palm stearin and high-oleic sunflower seed oil is 55-62:1-5:35-40. Preferably, the use and method include one or more of the following: increasing the protein expression of tight junction-related proteins (such as occludin, claudin, and ZO-1) in the mucosa of the duodenum, jejunum, and ileum; decreasing the CRF content in intestinal tissue; strengthening or improving the mechanical barrier in the intestinal tract of piglets; increasing the concentrations of IgG, IgA, and IgM in the jejunum; increasing the concentration of IgA in the ileum; and upregulating the protein expression of TLR4 and NF-κB in the duodenum, jejunum, and ileum. To regulate inflammatory cytokines (such as TNF-α, IL-1β, IL-6, and / or IL-10) to maintain immune homeostasis in the ileum; to maintain mucin levels in the intestinal mucosa and maintain immune homeostasis in the ileum; to increase Ki67 protein expression in intestinal epithelial cells, promote the proliferation of intestinal epithelial cells, improve the mechanical barrier of the intestine, and promote intestinal development; to activate the mTOR signaling pathway, increase the expression of activated mTOR protein in small intestinal cells, and promote cell proliferation and tissue development;It increases the level of activated S6 kinase in small intestinal cells, restores cell proliferation and protein metabolism in small intestinal tissue, and promotes tissue development; it increases the level of digestive enzymes (including maltase, aminopeptidase, and / or sucrase) in the small intestine, and promotes nutrient absorption; it increases the 5-hydroxytryptamine content in the duodenum, jejunum, and ileum, and the substance P content in the ileum, regulates intestinal peristalsis, promotes the contraction of smooth muscle in the digestive tract, suppresses gastric acid and bile secretion, regulates local gastrointestinal blood flow, enhances small intestinal function, and Downregulate the expression levels of intravesicular mitochondrial autophagy-related proteins (e.g., ULK1, TFEB, and / or parkin) to alleviate mitochondrial dysfunction and maintain energy homeostasis of intestinal cells; upregulate the levels of lipid synthesis-related transcription factors (including PPARγ and / or SREBP-1) to improve lipid absorption and anabolism in the small intestine and maintain energy homeostasis of intestinal cells; upregulate the content of type I and type II muscle fibers in muscle tissue and the expression levels of mTOR proteins, A It reduces the relative content of MPK and PGC1-α, alleviates the energy state of muscle tissue, promotes cell proliferation and tissue development, increases muscle fiber content, inhibits the conversion of type II muscle fibers to type I muscle fibers, increases muscle mass, and promotes overall muscle tissue development; it upregulates the expression of SREBP-1 in muscle tissue, increases lipid uptake and utilization by muscle tissue, improves energy state, and promotes muscle tissue development; it upregulates the expression of activated mTOR and decreases the expression of Prdm16 and Irisin, thereby suppressing lipolysis, increasing lipid synthesis, and promoting adipose tissue development; it upregulates the level of SERBP-1 in adipose tissue, maintains APOB levels, increases lipid synthesis in adipose tissue, promotes lipid transport in the body, and maintains the energy balance of adipose tissue and the body; it maintains the serum GSH-PX content, improves the body's overall antioxidant capacity, maintains overall redox equilibrium, reduces blood HIS, jejunal IgE, ileal IgE and HIS, and reduces allergic reactions in the body and in the jejunum and ileum. ;

[0052] In this specification, "individual" or "subject" primarily refers to mammals such as humans, livestock (e.g., pigs, cattle, sheep, horses, camels, donkeys, etc.), research mammals (e.g., rats, mice, apes, monkeys, dogs, etc.), animals kept by humans, or wild animals. This application does not exclude individuals other than mammals, such as poultry or aquatic organisms.

[0053] In this specification, an effective dose refers to the amount administered over a period of time to achieve the intended purpose. Those skilled in the art can determine the effective dose for different individuals, different purposes, or symptoms using conventional methods in the art.

[0054] The formulations described herein may be foods, for example, dietary supplements. Dietary supplements may contain other ingredients found in conventional dietary supplements, such as dietary cellulose, vitamins, and minerals. Dietary supplements may be provided in the form of capsules, granules, powders, tablets, drops or lumps, capsules, pellets, semi-emulsions or emulsions, etc. Examples of foods include beverages, dairy products, confectionery, chocolate, pastries, snack foods, meat products, egg products, refrigerated foods, pet food, and animal feed. Examples of dairy products include powdered milk, liquid milk, milk tablets, and yogurt. Examples of pastries include biscuits, bread, and cakes. Examples of beverages include carbonated drinks, soda water, fruit-flavored water, plum drinks, low-sugar drinks, mineral drinks, malt milk powder, milk tea, and coffee. Examples of refrigerated foods include ice pops, frozen desserts, ice cream, and pudding.

[0055] In addition to containing the odd-carbon fatty acids described herein, the pharmaceuticals described herein may further contain pharmaceutically acceptable carriers that are well known in the art. [Examples]

[0056] The present invention will be further described below with reference to specific examples. It should be understood that these examples are for illustrative purposes only and do not limit the scope of the present invention. Experimental methods in the following examples where specific conditions are not specified are typically carried out under conventional conditions or conditions recommended by the manufacturer. Unless otherwise specified, percentages and parts are based on weight.

[0057] Example 1 1. Basic experimental procedure After mixing the oils and fats listed in the table below, chemical transesterification was performed to ensure that the fatty acids were uniformly distributed on the glycerol backbone, eliminating the influence of differences in fatty acid positions on digestion, absorption, and function. The resulting oils and fats were purified and prepared into an oil-in-water emulsion. This oil-in-water emulsion was spray-dried to obtain an oil powder. The resulting oil powder was fed to piglets as a nutritional supplement. TIFF2026522594000001.tif22170

[0058] The feeding method for the piglets was as follows: The piglets were weaned at 7 days old and fed commercially available powdered milk for 6 days. After that, for the first feeding each day, liquid milk was mixed with oil powder and given after the oil powder had dissolved. At other times, commercially available powdered milk was given as usual. This feeding was carried out for a total of 15 days.

[0059] 2. Preparation of triglycerides containing odd-carbon fatty acids Glycerol (Yihai Kerry) and pentadecanoic acid (Titan Platform, purchased from Adamas, purity ≥95%) were mixed in a 1:4 molar ratio and heated to 70°C to mix uniformly, forming the reaction substrate. Immobilized enzyme NOVO435 (Novozymes) was added at 10% by weight of the substrate, and the mixture was reacted at 70°C, 300 rpm, and under a vacuum of ≤10 mbar for 15 hours to obtain the crude oil product. The obtained crude oil product was subjected to molecular distillation separation, and the heavy phase was glyceryl pentadecanoate (C15-TAG) with a purity of >98%.

[0060] Using the method described above, glyceryltriundecanoic acid, glyceryltritridecanoic acid, and glyceryltriheptadecanoic acid were prepared using undecanoic acid (adamas, purity ≥99%), tridecanoic acid (accelera, purity ≥95%), and heptadecanoic acid (adamas, purity ≥98%), respectively.

[0061] 3. Preparation of oils and fats fats and oils 1 Hard ST (Yihai Kerry, batch RBDHard ST321, acid value 0.04 mg / KOH / g) and high-oleic sunflower seed oil (Yihai Kerry, model finished product first grade) were uniformly melted and mixed in a mass ratio of 73:27. Subsequently, chemical transesterification was performed to ensure that the fatty acids were uniformly dispersed on the glycerol backbone. The chemical transesterification procedure was as follows: First, dehydration was carried out under vacuum at 110°C for 1 hour, then sodium methoxide was added in an amount of 0.2% of the oil's weight, and the reaction was carried out under vacuum at 110°C for 1 hour. The temperature was lowered to below 80°C, and citric acid (prepared as a 10% citric acid solution) was added in an amount equal to 1.8 times the mass of sodium methoxide. After stirring, the mixture was poured into a separatory funnel, washed with hot water until neutral, and then dehydrated under vacuum at 110°C. The oil obtained as described above can be purified according to conventional oil refining methods. In this example, oil 1 was obtained by purification using the following oil refining method.

[0062] Methods for refining oils and fats: 1. 500g of oil was weighed and added to a 2L glass-jacketed reactor. After melting by natural heating, the temperature was maintained at 60°C. The stirring speed was 200 rpm, and the entire process was protected with nitrogen gas. The AV (acid value) and PV (peroxide value) were measured. 2. Wash with water, add citric acid solution dropwise (15% water, 0.5‰ citric acid), and stir at 200 rpm for 5 minutes. Stop stirring and let the mixture stand for 4 hours to allow precipitation. After precipitation is complete, drain the lower aqueous phase. Then, gradually add water dropwise (15% water), and stir at 200 rpm for 5 minutes. Stop stirring and let the mixture stand for 4 hours to allow precipitation. After precipitation is complete, drain the lower aqueous phase. 3. Alkali purification was performed. Samples were taken, AV and PV were measured, and the amount of alkali to be added was calculated. Amount of alkali to be added = Theoretical alkali amount (0.713 × amount of oil (tons) × acid value / alkali concentration 0.93) + excess alkali amount (weight of crude oil × 0.0005), Amount of water to be added (kg) = Amount of alkali to be added (kg) × 40. An alkaline solution was prepared using water and alkali. The oil was heated to 60°C. Stirring was started at 100 rpm, and the alkaline solution was added within 5 minutes. After the addition was completed, the mixture was rapidly stirred for 5 minutes and left for 4-6 hours to form a precipitate. After precipitation was complete, the lower aqueous phase was discharged. Washing with brine: Water (15% added) and sodium chloride (0.5‰ added) were gradually added dropwise to the algal oil. The stirring speed was 100 rpm. After stirring for 3 minutes, stirring was stopped, and precipitation was left for 3 hours. After precipitation was complete, the lower aqueous phase was discharged. Washing with alkaline water: Water (15% added) and alkali (0.2‰ added) were gradually added dropwise to the oil. The stirring speed was set to 100 rpm. After stirring for 3 minutes, stirring was stopped and the mixture was allowed to settle for 3 hours. After settling was complete, the lower aqueous phase was drained and the washing with alkaline water was repeated twice. Washing with water: 15% water was added. After adding, stirring was stopped for 3 minutes, then the mixture was allowed to settle for 3 hours. After settling was complete, the lower aqueous phase was drained. Washing with water was performed a total of two times. 4. Decolorization. Decolorization and deodorization were carried out according to conventional methods. The decolorization temperature was 105°C. Chalk was added as a decolorization adsorbent at a concentration of approximately 2% of the oil weight. After decolorization at a vacuum of 10 mbar for 0.5 hours, filtration was performed. 5. Deodorization was performed for 2 hours at a temperature of 200°C and a vacuum of 5 mbar while introducing nitrogen gas, and after purification, refined oil was obtained.

[0063] fats and oils 2 OCFA algae oil (Yihai Kerry) and high-oleic sunflower seed oil (Yihai Kerry) were dissolved in a mass ratio of 92:8 and mixed uniformly. Next, chemical transesterification was performed so that the fatty acids were uniformly distributed on the glycerol backbone, and the resulting oil was purified. The chemical transesterification method and oil purification method are the same as those for oil 1 (in the animal experiments in this application, the oil obtained by this manufacturing method was used).

[0064] Oil 2 can also be prepared by the following method: Glyceryl triundodecanoate, glyceryl tritridecanoate, glyceryl tripentadecanoate, and glyceryl triheptadecanoate prepared by the method described above were melted and homogeneously mixed with DHA algae oil (Qingdao Keyuan, obtained by refining purchased crude oil; for refining methods, see "Optimization of the refining processes for microalgae DHA" by Huang Huaixin. Crude oil batch is MKD120056) and high oleic sunflower seed oil (Yihai Kerry) in a mass ratio of 1:3:47:7:35:7. Next, chemical transesterification was performed so that the fatty acids were uniformly distributed on the glycerol backbone, and the resulting oil was purified. The chemical transesterification and oil purification methods are the same as for oil 1.

[0065] fats and oils 3 C15-TAG, hard ST (Yihai Kerry), and high-oleic sunflower seed oil (Yihai Kerry) were melted and uniformly mixed in a mass ratio of 59:4:37. Next, chemical transesterification was performed so that the fatty acids were uniformly distributed on the glycerol backbone. The chemical transesterification and oil refining methods were the same as those for oil 1.

[0066] The hard ST and high-oleic sunflower seed oil used in the above oils 1-3 were products from the same manufacturer and in the same batch.

[0067] 4. Fatty acid composition of oils and fats The major fatty acid compositions of the above-mentioned hard ST, high-oleic sunflower seed oil, DHA algae oil, and OCFA algae oil, as well as the major fatty acid compositions of oils 1-3, were measured using the third method, i.e., the "normalization method," in "GB5009.168-2016 Food Safety National Standard Determination of Fatty Acids in Foods." The results are shown in Tables 1-1 and 1-2, respectively.

[0068] [Table 1-1]

[0069] [Table 1-2]

[0070] 5. Preparation of oil and fat supplements 15 g of monoglyceride (Yihai Kerry, model DMG-CF01), 15 g of phospholipid (Yihai Kerry, non-genetically modified soybean phospholipid), and 300 g of oil (i.e., oil 1, 2, or 3 above) were mixed and stirred at 60°C until dissolved and homogeneous. An aqueous solution of 1.08 kg of lactose and 97.5 g of sodium caseinate dissolved in 3.5 kg of pure water was added, and the mixture was subjected to high-speed shearing at 12,000 rpm for 8 minutes, followed by two consecutive high-pressure homogenization cycles at a pressure of 300 bar to prepare an emulsion. The emulsion was spray-dried at an inlet temperature of 180°C and an outlet temperature of 90°C. Thus, oil supplements 1 to 3 were obtained. The oils used in oil supplements 1 to 3 are shown in Table 2 below.

[0071] [Table 2]

[0072] 6. Animal experiments Experimental Animals: In the experiment, healthy "Du×Chang×Da" weaned piglets were selected at 7 days of age and divided into three groups of 10 piglets each, according to a fully randomized block design based on the principles of similarity in weight, sex, and genetic background (see Table 3). An additional group of 10 homologous piglets, G0, which were breastfed at a pig farm, were added to each group. At 7 days of age, the piglets were transferred from the pig farm to the Institute of Subtropical Agricultural Ecology, Chinese Academy of Sciences, where they were fed commercially available piglet formula (Tangrengin) and allowed to adapt to the environment. Daily management was carried out according to the management patterns of a large-scale pig farm. After 6 days of pre-feeding, the above nutritional supplements were added daily to the first meal, based on the basic formula milk (Tangrengin). The piglets were fed until 28 days of age, then fasted for 12 hours, slaughtered, and samples were taken. Samples were taken from 8 piglets in each group and measured and analyzed. All relevant operating procedures meet the requirements of the Animal Welfare and Ethics Committee for Animal Experiments of the Institute of Subtropical Agricultural Ecology, Chinese Academy of Sciences.

[0073] [Table 3]

[0074] The method for determining the nutritional parameters described here is as follows: Measurement of serum biochemical markers: Using a commercially available kit (Leadman Biotech Limited, Beijing, China) and a biochemical analyzer (Beckman CX4, Beckman Coulter, Germany), the concentrations of total protein (TP), albumin (ALB), blood urea nitrogen (BUN), creatinine (CRE), blood glucose (GLU), insulin (INS) (fasting insulin resistance index = fasting blood glucose × fasting insulin / 22.5, fasting blood glucose unit: mmol / L, fasting insulin unit: μU / mL), immunoglobulins IgG and IgM, HDL-C, LDL-C, serum glutamate aminotransferase (ALT), serum aspartate aminotransferase (AST), serum total triglycerides (TG), total cholesterol (CHOL), D-lactic acid, and total bile acids (TBA) were analyzed.

[0075] Indicators for RT-PCR testing: IL-1β, IL-6, TNF-α, TLR4, NF-κB, MUC-2 in the duodenum, jejunum, and ileum. SREBP-1C, PPARγ, APOB, FAS, ACC, PPARα, ACOX, CPT-1α, HSL, etc. in the longissimus dorsi muscle and back fat. For information on the RT-QPCR method, please refer to "B. Song, Dietary leucine supplementation improves intestinal health of mice through intestinal SIgA secretion, 2019".

[0076] Indicators for Western blot analysis: Ki-67, Occludin, Claudin, ZO-1, TLR4, NK-κB, mTOR, ULK1, TFEB, SREBP1, PPARγ, HIF1α, PINK, Parkin, and p-mTOR in each intestinal segment. p-mTOR, Prdm16, and Irisin in dorsal fat and perirenal fat. Slow MyHC, Fast MyHC, mTOR, AMPK, and PGC-1α in dorsal muscle. For the Western blot analysis method, refer to "B. Song, Dietary leucine supplementation improves intestinal health of mice through intestinal SIgA secretion, 2019".

[0077] Indicators for the ELISA assay: Grinding tissue was determined according to the manufacturer's instructions (Nanjing Jiancheng Bioengineering Institute, Jiangsu Province, China). A commercially available porcine ELISA kit (Cusabio Life Science, Inc., Wuhan, China) was used to measure the concentrations of malondialdehyde MDA, glutathione peroxidase GSH-PX, superoxide dismutase SOD, insulin and glucagon, stress hormones (cortisol and ACTH); D-xylose, IL-1β, IL-6, IL-10, and TNF-α in serum. Concentrations of IL-1β, IL-6, IL-10, and TNF-α in each intestinal segment. IgA, IgG, and IgM in the spleen, jejunum, and ileum. Activity of aminopeptidase N, sucrase, and maltase, and expression of 5-hydroxytryptamine, norepinephrine, substance P, and adrenocorticotropin-releasing factor in each intestinal segment. IgE and HIS in plasma, spleen, and each intestinal segment.

[0078] Intestinal morphology: Referencing "JY 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". Morphological analysis was performed on fixed sections of the duodenum, jejunum, and ileum by hematoxylin-eosin staining. Parameters such as villi height (VH) and crypt depth (CD) were measured under a microscope and measured using CaseViewer software. The ratio of VH to CD was calculated. Referencing "Y. Xiao, Ellagic acid alleviatesoxidative stress by mediating Nrf2 signaling pathways and protects against paraquat-induced intestinal injury in piglets". Intestinal sections were cooled and fixed with 2.5% glutaraldehyde and analyzed using scanning electron microscopy and transmission electron microscopy.

[0079] 7.Results 7.1 Gut Health (1) Mechanical barrier of the intestinal tract Table 4 and Figure 1 show the effects of daily feeding treatments on the expression of tight junction proteins in the intestinal tract of piglets. As can be seen from Figure 1, compared to the breast milk group (G0 group), the G1 group showed a significant decrease in the protein expression of tight junction-related proteins (occludin, claudin, ZO-1) in the duodenal, jejunal, and ileal mucosa (P<0.05). Compared to the G1 group, the G3 group showed a significant increase in the protein expression of tight junction-related proteins (occludin, claudin, ZO-1) in the duodenal, jejunal, and ileal mucosa (P<0.05). Compared to the G1 group, the G2 group also showed an increase in the protein expression of tight junction-related proteins (occludin, claudin, ZO-1) in the duodenal, jejunal, and ileal mucosa. These results indicate that supplementing the diet with odd-carbon fatty acids, compared to even-carbon fatty acids, promotes the expression of tight junction proteins in intestinal epithelial cells and improves the mechanical barrier of the piglet intestinal tract; the higher the proportion of C15 in the composition of odd-carbon fatty acids, the more the mechanical barrier of the piglet intestinal tract can be enhanced by promoting the expression of tight junction proteins (duodenal occludin, duodenal claudin, duodenal ZO-1, jejunal occludin, jejunal claudin, ileal occludin, ileal claudin, ileal ZO-1, etc.) in intestinal epithelial cells.

[0080] [Table 4]

[0081] Table 5 and Figure 2 show the effects of daily feed administration on levels of releasing hormones in the intestinal tract of piglets. Corticotropin-releasing hormone (CRF) is a releasing hormone involved in the stress response and is primarily used to promote the synthesis of adrenocorticotropic hormone in the pituitary gland. While CRF is often thought to be associated only with central secretion, the evidence in this application shows that peripheral release of CRF plays a crucial role in regulating gastrointestinal permeability and is part of the gut-brain axis connection. As can be seen in Figure 2, the CRF content in the ileum of piglets in the G1 group was significantly increased compared to the breast milk group (G0 group) (P<0.05), suggesting a possible weakening of the mechanical barrier of the intestinal wall at the end of the small intestine. However, compared to the G1 group, the CRF content in the ileal tissue of piglets in the G3 group was significantly decreased (P<0.05), and the CRF content in the ileal tissue of piglets in the G2 group was also decreased compared to the G1 group. These results indicate that supplementing the diet with odd-carbon fatty acids, compared to even-carbon fatty acids, reduces CRF content in intestinal tissue and strengthens or improves the mechanical barrier function of the intestinal tract in piglets.

[0082] [Table 5]

[0083] (2) Immune homeostasis in the intestinal tract Table 6-1 and Figure 3 show the effects of daily feed administration on immunoglobulins in the jejunum of piglets. Immunoglobulins are a type of protein that possesses antibody activity in the human body. Immunoglobulins are an important component of the body's resistance to disease. They have antibacterial and antiviral properties and promote phagocytosis of cells. In addition, through synergistic effects with complement, they can kill or lyse pathogenic microorganisms. Typically, IgG, IgM, and IgA are detected. IgG accounts for 75% of total immunoglobulins and is the most important antibody that persists the longest in the primary immune response. IgA is the first line of defense against pathogen invasion, and IgM plays an important role in early defense. As shown in Figure 3, compared to the G1 group, IgG, IgA, and IgM in the jejunum of the G3 group were all significantly increased (P<0.05); compared to the G1 group, jejunal IgG protein and IgM protein were also increased in the G2 group. These results suggest that dietary supplementation with odd-carbon fatty acids, compared to even-carbon fatty acids, can maintain jejunal immune homeostasis by increasing the amount of jejunal immunoglobulins.

[0084] [Table 6-1]

[0085] Table 6-2 and Figure 4 show the effects of daily feed administration on ileal immunoglobulins in piglets. As can be seen from Figure 4, ileal IgA was significantly increased in the G3 group compared to the G1 group (P<0.05), while no significant changes were observed in IgG and IgM. IgA is the first line of defense against pathogen invasion, and this suggests that dietary supplementation with odd-carbon fatty acids, compared to even-carbon fatty acids, can enhance jejunal immunity and improve the ileum's ability to defend against pathogen invasion by increasing the ileal immunoglobulin IgA content.

[0086] [Table 6-2]

[0087] Table 7 and Figure 5 show the effects of daily feed administration on the TLR4 / NF-κB signaling pathway in the intestinal tract of piglets. Inflammatory responses are an important immune defense mechanism of the body. Normal inflammatory responses are a manifestation of the body's immunity and are beneficial to the body. TLR4 / NF-κB is an inflammatory response signaling pathway in the body. As can be seen from Figure 5, compared to the breast milk group (G0 group), the protein expression levels of inflammation-related genes (TLR4 and NF-κB) in the duodenum, jejunum, and ileum of piglets in the G1 group were significantly reduced (P<0.05), indicating that dietary changes led to changes in intestinal immune homeostasis. Compared to the G1 group, the protein expression levels of TLR4 and NF-κB in the duodenum, jejunum, and ileum were significantly increased in the G3 group (P<0.05); compared to the G1 group, the protein expression levels of TLR4 and NF-κB in the duodenum, jejunum, and ileum were also increased in the G2 group. These results suggest that dietary supplementation of odd-carbon fatty acids, compared to even-carbon fatty acids, can maintain immune homeostasis in the gut by regulating the expression of the TLR4 / NK-κB signaling pathway; and that a higher proportion of C15 in the composition of odd-carbon fatty acids is associated with maintaining immune homeostasis in the gut by regulating the expression of the TLR4 / NK-κB signaling pathway.

[0088] [Table 7]

[0089] Table 8 and Figure 6 show the effects of daily feed administration on ileal inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-10) in piglets. Inflammation prompts damaged cells to release chemicals. These released chemicals are commonly called inflammatory cytokines. Cytokines act as intercellular information molecules, interacting with cells of the immune system, regulating the body's response to disease and infection, and mediating the activity of normal cells in the body. As can be seen from Figure 6, ileal inflammatory cytokines were altered in the G1 group compared to the breast milk group (G0 group) (P<0.05), indicating that dietary changes led to changes in ileal immune homeostasis. Compared to G1, the G3 and G2 groups were able to regulate inflammatory cytokines to a degree that approached those of the breast milk group. This indicates that dietary supplementation with odd-carbon fatty acids, compared to even-carbon fatty acids, can maintain ileal immune homeostasis by regulating inflammatory cytokines.

[0090] [Table 8]

[0091] Table 9 and Figure 7 show the effect of daily feeding on ileal mucin 2 concentration in piglets. Mucin 2 (MUC-2) is one of the main components of the intestinal mucus layer and is secreted by goblet cells. It forms a colloidal matrix containing antimicrobial molecules and effectively prevents the invasion of bacteria and viruses into the intestinal mucosa. As shown in Figure 7, the expression level of ileal mucin 2 in the G1 group was significantly reduced compared to the breast milk group (G0 group), suggesting a decrease in the immune function of the ileal mucosa (P<0.05). However, in the G2 and G3 groups, the expression level of ileal mucin 2 was regulated to the level of the breast milk group. This indicates that dietary supplementation with odd-carbon fatty acids, compared to even-carbon fatty acids, can jointly maintain ileal immune homeostasis by maintaining mucin levels in the mucosa.

[0092] [Table 9]

[0093] Table 10 and Figure 37 show the effect of daily feeding treatments on the relative expression of hypoxia-inducible factor HIF-1α in the intestinal tract of piglets. The intestinal environment is normally hypoxic. HIF-1α plays an important role in maintaining intestinal homeostasis and host-microbe interactions as a major regulator of cellular responses to hypoxia. For example, some of its target genes may be 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. This indicates that dietary supplementation with odd-carbon fatty acids, compared to even-carbon fatty acids, increases HIF-1α expression in the intestinal tract, promoting the survival of intestinal cells in a hypoxic intestinal environment and contributing to the maintenance of intestinal homeostasis.

[0094] [Table 10]

[0095] (3) Development of the intestinal tract Figures 38-42 show the measurement results regarding intestinal development. Scanning electron microscopy (Figure 38) shows that the intestinal villi of piglets from groups G2 and G3 were longer, thicker, and denser than those of piglets from group G1. In particular, the intestinal villi of group G3 were comparable to those of group G0. Figure 39 shows the morphology of the intestinal tract as determined by HE staining. The duodenum, jejunum, and ileum of piglets from groups G2 and G3 all showed better intestinal morphology than that of group G1, and were closer to the morphology of piglets from group G0 that were breastfed. The functional unit of the small intestine is the villi. The longer the villi, the more absorptive cells there are, and the deeper the crypts, the less contact there is between intestinal epithelial cells and nutrients. Small intestinal villi height (VH) and the ratio of villi height to crypt depth (CD) (VH:CD) are commonly used as indicators to evaluate the developmental state of the small intestine. As can be seen from the results in Figures 40-42, the VH and VH:CD in the intestinal tract of piglets in the G1 group were both significantly lower than in the G0 group (both P<0.05), and the CD was deeper (both P<0.05), indicating that feeding with powdered milk may have adverse effects on the intestinal tract of piglets. As shown in Figure 40 and Table 11-1, in the duodenum, the VH:CD in the G2 and G3 groups was significantly higher than in the G1 group (P<0.05), and there were no significant differences in VH, CD, or VH:CD between the G2 and G3 groups compared to the G0 group. As shown in Figure 41 and Table 11-2, in the jejunum, the VH:CD in the G2 group was significantly higher than in the G1 group (P<0.05), and the CD was significantly lower than in the G1 group (P<0.05). VH and VH:CD were significantly higher in the G3 group than in the G1 group (P<0.05), and CD was significantly lower in the G3 group than in the G1 group (P<0.05). Furthermore, none of the above indicators were significantly different from those of the G0 group. As shown in Figure 42 and Table 11-3, in the ileum, VH:CD was significantly higher in the G2 and G3 groups than in the G1 group (P<0.05), and CD was significantly lower in the G3 group than in the G1 group (P<0.05). Furthermore, the aforementioned indicators were close to those of the G0 group. In summary, the above results demonstrate that odd-carbon fatty acids are beneficial for improving intestinal morphology, increasing VH and VH:CD, decreasing CD, and promoting intestinal development, and that they can bring the intestinal development of animals fed formula milk to a level comparable to that of breastfed animals.

[0096] [Table 11-1]

[0097] [Table 11-2]

[0098] [Table 11-3]

[0099] Table 12 and Figure 8 show the effect of daily feed administration on the proliferation of intestinal epithelial cells in piglets. Ki67 is an antigen associated with proliferating cells. Its function is closely related to mitosis and is essential for cell proliferation. Higher levels of Ki67 expression indicate more active cell proliferation. As can be seen from Figure 8, Ki67 protein expression in intestinal epithelial cells of group G3 was significantly higher than in group G1 (P<0.05), and Ki67 protein expression in intestinal epithelial cells of group G2 was significantly higher than in group G1. These results indicate that supplementing the diet with odd-carbon fatty acids, compared to even-carbon fatty acids, improves the mechanical barrier of the intestine, promotes the proliferation of intestinal epithelial cells, and accelerates intestinal development; in the composition of odd-carbon fatty acids, a higher proportion of C15 can improve the mechanical barrier of the intestine, promote the proliferation of intestinal epithelial cells, and accelerate intestinal development.

[0100] [Table 12]

[0101] Table 13 and Figure 9 show the effects of daily feeding on mTOR protein levels in the small intestine of piglets. mTOR (mammalian target of rapamycin) protein is a kinase regulated by growth factors and environmental nutrient levels. It plays a crucial role in regulating cellular processes and tissue development by interacting with various proteins and activating or inhibiting downstream signaling pathways, thereby promoting ribosome formation and the synthesis of proteins, lipids, and nucleic acids, inhibiting cellular autophagy, and promoting cell growth and proliferation. Compared to the breast milk group (G0 group), the expression level of phosphorylated (activated) mTOR protein in the G1 group was significantly reduced (P<0.05), indicating inhibition of normal cell proliferation activity. In the G3 group, the expression level of activated mTOR protein in small intestinal cells increased to levels comparable to or close to those of the breast milk group; also, the expression level of activated mTOR protein in small intestinal cells of the G2 group was higher than that of the G1 group. These results indicate that dietary supplements of odd-chain fatty acids activate the mTOR signaling pathway, promoting cell growth and tissue development; the higher the proportion of C15 in the odd-chain fatty acid composition, the more the mTOR signaling pathway is activated, promoting cell growth and tissue development.

[0102] [Table 13]

[0103] 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 type of protein kinase involved in signal transduction, activated by the mTOR protein, and regulates cell proliferation and tissue development by controlling protein synthesis and ribosome production. Similar to the expression status of the mTOR protein, the level of phosphorylated (activated) S6 kinase in the G1 group was significantly reduced compared to the breast milk group (G0 group) (P<0.05), indicating that normal cell proliferation was inhibited. In the G3 group, the level of activated S6 kinase in small intestinal cells increased to levels equivalent to or close to those of the breast milk group, and the level of activated S6 kinase in small intestinal cells of the G2 group was also significantly higher than in the G1 group. This suggests that dietary supplementation with odd-carbon fatty acids can suppress cell proliferation and protein metabolism in small intestinal tissue and promote tissue development. This regulation may be mediated through the mTOR signaling pathway. In the composition of odd-carbon chain fatty acids, a higher proportion of C15 may suppress cell proliferation and protein metabolism in small intestinal tissue, and promote tissue development.

[0104] [Table 14]

[0105] Table 15 and Figure 11 show the effects of daily feed administration on digestive enzyme levels in the small intestine of piglets. Maltase, aminopeptidase (APN), and sucrase (invertase) are digestive enzymes present at the brush border of the small intestine. They can reflect the digestive and absorptive function of the intestinal tract and are important indicators of intestinal physiological function, development, and maturation. As can be seen from Figure 11, the levels of digestive enzymes in the G1 group were significantly different from those in the breast milk group (G0 group) (P<0.05), indicating that the change in diet led to a change in the digestive capacity of the small intestine. In the G3 group, the levels of digestive enzymes in the small intestine may have risen to levels that reached or exceeded those of the breast milk group. This suggests that supplementing the diet with odd-carbon fatty acids can increase the levels of digestive enzymes in the small intestine, aiding in the full absorption of nutrients.

[0106] [Table 15]

[0107] Table 16 and Figure 12 show the effects of daily feed administration on the levels of neurotransmitters and neuropeptides in the small intestine of piglets. 5-hydroxytryptamine (5-HT) is a type of monoamine neurotransmitter. It is mainly synthesized in chromaffin cells of the small intestine of animals, and is also present in small amounts in platelets and the central nervous system, performing various functions in various tissues. Approximately 90% of 5-hydroxytryptamine in the body of animals is present in gastrointestinal cells and the intermuscular plexus of the enteroin, and is involved in regulating intestinal peristalsis. Substance P (SP) is also widely distributed in the digestive tract and mainly has effects such as promoting the contraction of digestive tract smooth muscle, suppressing the secretion of gastric acid and bile, and regulating local blood flow in the digestive tract. As shown in the figure above, the content of neurotransmitters and neuropeptides in the small intestine of the G1 group was equivalent to or slightly reduced compared to the breast milk group (G0 group). However, in the G3 group, 5-hydroxytryptamine concentrations in the duodenum, jejunum, and ileum, as well as the amount of substance P in the ileum, increased significantly to levels exceeding those of the breast milk group, while in the G2 group, 5-hydroxytryptamine concentration in the duodenum increased significantly. This suggests that dietary supplementation with odd-carbon fatty acids can enhance small intestinal function by increasing levels of gut-brain peptides related to the gut-brain axis.

[0108] [Table 16]

[0109] (4) Energy metabolism in the intestinal tract Table 17 and Figure 13 show the effects of daily feeding treatments on the level of mitochondrial autophagy in the small intestine of piglets. Mitochondrial autophagy is a programmed mitochondrial degradation process within cells, primarily occurring in damaged or defective mitochondria and used to prevent cellular abnormalities resulting from the accumulation of dysfunctional mitochondria. As shown in Figure 13, the expression levels of major mitochondrial autophagy proteins (ULK1, TFEB, Parkin) were significantly increased in the G1 group compared to the breast milk group (G0 group) (P<0.05), suggesting an excessive accumulation of abnormal mitochondria within the cells. In the G2 and G3 groups, the expression levels of intracellular mitochondrial autophagy-related proteins could be downregulated to levels comparable to those of the breast milk group. This indicates that dietary supplementation with odd-carbon fatty acids, compared to even-carbon fatty acids, can mitigate mitochondrial dysfunction, which is considered beneficial for maintaining energy homeostasis in intestinal cells; the higher the proportion of C15 in the composition of odd-carbon fatty acids, the more mitochondrial dysfunction is mitigated, which is considered beneficial for maintaining energy homeostasis in intestinal cells.

[0110] [Table 17]

[0111] Table 18 and Figure 14 show the effect of daily feed administration on lipid metabolism levels in the intestinal tract of piglets. Lipids are essential functional substances for the body and cells and are the primary form of energy storage. The activity of lipid metabolism can reflect the overall energy state of the tissue. PPARγ and SREBP-1 are transcription factors involved in intracellular lipid metabolism and are closely related to lipid uptake and synthesis. As can be seen from the figure above, the content of PPARγ and SREBP-1 in the duodenum and jejunum of the G1 group was significantly reduced compared to the breast milk group (G0 group) (P<0.05), suggesting inhibited lipid synthesis and abnormalities in the cellular energy state. The G2 and G3 groups were able to upregulate the levels of transcription factors related to lipid synthesis, and to some extent, their levels reached or approached those of the breast milk group. This indicates that dietary supplementation of odd-carbon fatty acids promotes lipid absorption and assimilation in the small intestine of piglets, which is beneficial for maintaining energy homeostasis of intestinal cells; it is thought that the higher the proportion of C15 in the composition of odd-carbon fatty acids, the more lipid absorption and assimilation in the small intestine of piglets is promoted, which is beneficial for maintaining energy homeostasis of intestinal cells.

[0112] [Table 18]

[0113] (5) Muscle tissue development and metabolism Muscle tissue is composed of muscle fibers (cells), which are classified into type I fibers (MYHC I) and type II fibers (MYHC II) based on differences in appearance and function. Type I fibers are also called red muscle fibers, slow-twitch fibers, or slow-oxidation fibers. These muscle fibers have a slow contraction speed, low force, high oxygen utilization rate, and excellent endurance. Type II fibers are called white muscle fibers, fast-twitch fibers, or fast-glycolytic fibers. They mainly supply short-term energy via glycolysis and have low endurance, but are highly effective in improving explosive power and speed during exercise, and are a major factor in determining muscle strength and speed. Also, the cross-sectional area of ​​fast-twitch fibers is relatively thick, and muscle tissue containing many fast-twitch fibers tends to develop well and become thick. In animal nutrition, the number of fast-twitch fibers is closely related to the yield of meat from animals and is an important indicator in animal production. mTOR also plays an important role in muscle tissue, controlling anabolic and catabolic signals in skeletal muscle and regulating muscle hypertrophy and atrophy. AMPK (AMP-activated protein kinase) is an energy-sensing enzyme that is activated when the cellular energy level is low (high ADP and AMP content). PCG1-α is a major regulator that induces the conversion of type II muscle fibers to type I muscle fibers.

[0114] As shown in Table 19 and Figure 15, compared to the breast milk group (G0 group), the G1 group's back muscle tissue showed a significant decrease in both the content of type I and type II muscle fibers and the expression level of mTOR protein (P<0.05), while the content of AMPK and PGC1-α was significantly increased (P<0.05). This indicates that the muscle tissue of the G1 group piglets was in a state of energy deficiency, leading to slow cell proliferation, continuous conversion from type II to type I muscle fibers, and consequently, a loss of body muscle mass. The G3 group significantly increased the content of type I and type II muscle fibers and the expression level of mTOR protein in muscle tissue (P<0.05), while simultaneously decreasing the relative content of AMPK and PGC1-α (P<0.05). The G2 group was also able to upregulate the content of type I and type II muscle fibers and the expression level of mTOR protein in muscle tissue, while simultaneously decreasing the relative content of AMPK and PGC1-α. This indicates that dietary supplementation with odd-carbon fatty acids can improve the energy state of muscle tissue, promote cell proliferation and tissue development, increase muscle fiber content, inhibit the conversion of type II muscle fibers to type I muscle fibers, increase muscle mass, and ultimately promote overall muscle tissue development; the higher the proportion of C15 in the composition of odd-carbon fatty acids, the better the energy state of muscle tissue, the more cell proliferation and tissue development are promoted, the more muscle fiber content is increased, the more the conversion of type II muscle fibers to type I muscle fibers is inhibited, the more muscle mass is increased, and ultimately promote overall muscle tissue development.

[0115] [Table 19]

[0116] Muscle is a major target organ for energy metabolism and glucose-lipid metabolism, and particularly active lipid metabolic processes are present during exercise. SREBP-1 is a transcription factor involved in intracellular lipid metabolism and is closely related to lipid uptake and synthesis. As shown in Table 20 and Figure 16, SREBP-1 content in the G1 group was reduced to some extent compared to the breast milk group (G0 group), but the reduction was not significant. However, in the G2 and G3 groups, the expression level of SREBP-1 in muscle tissue was significantly increased, indicating the presence of more active lipid anabolic activity within muscle tissue. This suggests that dietary supplementation of odd-carbon fatty acids promotes lipid absorption and utilization by muscle tissue, improves energy status, and is beneficial for muscle tissue development, which also leads to the aforementioned proliferation of muscle cells and increase in muscle mass.

[0117] [Table 20]

[0118] (6) Development and metabolism of adipose tissue Similar to other tissues mentioned earlier, mTOR proteins play a crucial role in lipid production and maintenance in adipose tissue, as well as in its development. The PR domain-containing protein-16 transcription factor (Prdm16) and irisin act on white adipocytes, inducing their conversion to brown adipocytes. Although brown adipose tissue is present in small amounts in adults, its heat-producing efficiency is very high, allowing even small amounts of brown fat to burn a large number of calories. Activated brown adipose tissue rapidly consumes glucose and fat to generate heat, which is important in combating obesity. Therefore, Prdm16 and irisin are molecular switches that control the browning of white fat and are involved in lipolysis. In the early stages of animal development, specific fat accumulations play a vital role in overall energy metabolism and homeostasis. As shown in Table 21 and Figure 17, compared to the breast milk group (G0 group), the activated mTOR protein content in the back fat and perirenal fat of piglets in the G1 group was significantly reduced (P<0.05), and the Prdm16 and Irisin content was significantly increased (P<0.05). This suggests that lipid synthesis and adipose tissue development were inhibited, the browning process of white fat was promoted, and clear lipolysis occurred. The G2 and G3 groups were able to significantly upregulate the expression of activated mTOR and reduce the expression levels of Prdm16 and Irisin. This indicates that dietary supplements of odd-carbon fatty acids can promote adipose tissue development by suppressing lipolysis and simultaneously promoting lipid synthesis. In the composition of odd-carbon fatty acids, the higher the proportion of C15, the more lipolysis is suppressed and lipid synthesis is promoted, thereby promoting adipose tissue development.

[0119] [Table 21]

[0120] Similarly, SREBP-1 is a transcription factor involved in intracellular lipid metabolism and is closely related to lipid uptake and synthesis. APOB (apolipoprotein) is a major component of lipoproteins and is responsible for lipid transport in various systems. As shown in Table 22 and Figure 18, compared to the breast milk group (G0 group), SREBP-1 levels were similar in piglets in the G1 group, but APOB levels were significantly reduced (P<0.05), suggesting that lipid transport may have been inhibited. In the G3 group, SREBP-1 levels in the adipose tissue of piglets were significantly increased, and APOB levels recovered to the level of the breast milk group (P<0.05). This means that supplementing with odd-carbon fatty acids from the diet increases lipid synthesis in adipose tissue, enhances lipid transport in the body, and helps maintain the energy balance of adipose tissue and the body.

[0121] [Table 22]

[0122] (7) The oxidation-reduction state in the body Glutathione peroxidase (GSH-PX) is a type of enzyme with peroxidase activity that plays a role in detoxification in living organisms. Its main biological functions are to reduce lipid peroxidation to corresponding alcohols and to reduce free hydrogen peroxide to water, thereby conferring antioxidant properties. As shown in Table 23 and Figure 19, the GSH-PX content of piglets in group G1 was significantly reduced compared to the breast milk group (group G0), suggesting that the antioxidant properties in the piglets' bodies were weakened, making them more susceptible to damage to cell structures and other substances caused by peroxides. In groups G2 and G3, the GSH-PX content in the serum of piglets increased significantly, recovering to levels close to those of the breast milk group. This means that supplementing with odd-carbon fatty acids through diet improves the body's overall antioxidant capacity and helps maintain overall redox equilibrium.

[0123] [Table 23]

[0124] (8) Allergic reactions in the body and intestinal tract The stronger the allergic reaction, the greater the release of IgE and HIS. As shown in Table 24 and Figure 20, the G3 group showed a significant decrease in serum HIS (P<0.05), jejunal IgE (P<0.05), ileal IgE (P<0.05), and HIS (P<0.05) compared to the G1 group, and the jejunal IgE and ileal IgE in the G2 group also decreased compared to the G1 group. This indicates that dietary supplementation with odd-carbon fatty acids is beneficial in reducing allergic reactions in the body and in the jejunum and ileum compared to even-carbon fatty acids.

[0125] [Table 24]

[0126] (10) Nutritional effects 4.1 Growth Performance As shown in Table 25 and Figure 21, dietary supplementation with odd-carbon fatty acids did not have a significant effect on the average daily increase in weight of piglets, average daily feed intake, or feed conversion rate.

[0127] [Table 25]

[0128] As shown in Table 26 and Figure 22, dietary supplementation with odd-carbon fatty acids did not affect the weight ratio of the liver, brain, cerebellum, and brainstem in piglets.

[0129] [Table 26]

[0130] The piglets' feces were observed daily throughout the experiment. No obvious diarrhea was observed in the piglets, and their growth was good throughout the entire process, indicating that supplementing with odd-carbon fatty acids in the feed did not cause diarrhea in the piglets.

[0131] A stress response is a nonspecific reaction in an individual triggered by various stressors, and prolonged stress responses can lead to pathological symptoms. When the body develops a stress response, blood levels of cortisol and adrenocorticotropic hormone (ACTH) increase. As shown in Table 27 and Figure 23, there was no significant difference in blood stress hormones (cortisol and ACTH) between the G1 and G3 groups (P>0.05), and no significant difference was observed in the G2 group either, indicating that dietary supplementation of odd-carbon fatty acids does not induce a stress response in suckling piglets.

[0132] [Table 27]

[0133] Abnormal lipid metabolism in the body can lead to increased levels of triglycerides (TG), cholesterol (CHOL), and low-density lipoprotein (LDL-C) in the blood, decreased high-density lipoprotein (HDL-C), and potential liver damage (liver damage increases glutamate oxaloacetate transaminase (AST) and glutamate pyruvate transaminase (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 in the G1 piglet group compared to the G2 and G3 groups, nor were there any significant differences in AST and ALT. This indicates that dietary supplementation with odd-carbon fatty acids does not cause abnormal lipid metabolism in the body compared to even-carbon fatty acids.

[0134] [Table 28]

[0135] Table 29 and Figure 25 show the effects of daily feed administration on indicators related to protein metabolism in the blood of piglets. As can be seen from Figure 25, supplementation with odd-carbon fatty acids in the feed did not affect protein metabolism in the blood.

[0136] [Table 29]

[0137] TNF-α is a cytokine involved in systemic inflammation, primarily secreted by macrophages. It can trigger acute reactions, promote fever, and induce cellular apoptosis. Serum TNF-α content serves, to some extent, as an indicator of the body's overall inflammatory state. Table 30 and Figure 26 show the effects of daily feeding treatments on key indicators of serum inflammation in piglets. As can be seen from Figure 26, dietary supplementation with odd-carbon fatty acids did not impose an additional burden on the overall inflammatory state of piglets compared to the G0 and G1 groups.

[0138] [Table 30]

[0139] Table 31 and Figure 27 show the effects of daily feed administration on immunoglobulins in the blood and spleen of piglets. As can be seen from the figure, there was no significant difference in IgG and IgM levels in the blood of piglets in groups G2 and G3 compared to group G1, and no difference was observed in IgA levels in the spleen. This indicates that dietary supplementation of odd-carbon fatty acids does not cause significant changes in the body's humoral immunity compared to even-carbon fatty acids.

[0140] [Table 31]

[0141] D-lactic acid (LACT) is the end product of metabolism by commensal bacteria in the gastrointestinal tract, and mammals lack an enzyme system to rapidly metabolize and break it down. Therefore, elevated blood D-lactic acid levels may reflect changes in intestinal permeability. Figure 28 shows the effect of daily feeding on blood D-lactic acid levels in piglets. As can be seen from Table 32 and Figure 28, there was no significant difference in serum D-lactic acid levels in piglets from groups G2 and G3 compared to group G1, indicating that dietary supplementation of odd-carbon fatty acids does not cause significant changes in the body's intestinal permeability compared to even-carbon fatty acids.

[0142] [Table 32]

[0143] Example 2 1. Basic experimental procedure In this experiment, pregnant female mice were given OCFA-containing oil and OCFA-free oil at normal daily feeding amounts and low-protein daily feeding amounts (abnormal diet), respectively (hard ST and high-oleic sunflower seed oil were mixed to eliminate the influence of DHA, SFA and UFA ratios in OCFA algae oil, and the ratio of n-3 to n-6 unsaturated fatty acids). Female mice were administered intragastricly on day 7.5 of gestation. From day 18.5 of gestation, the mice were fasted for 6 hours, sacrificed under ether anesthesia, and samples were collected.

[0144] The various measurement methods in this embodiment are the same as those in Example 1 unless otherwise specified.

[0145] 2. Preparation of oils and fats Oil 1:DHA algae oil (Qingdao Keyuan, obtained by refining purchased crude oil; for the refining method, refer to "Optimization of the refining processes for microalgae DHA" by Huang Huaixin; the crude oil batch was MKD120056) and hard ST (Yihai Kerry, the same batch of hard ST used in Example 1) were melted and uniformly mixed in a mass ratio of 1:1.2. Then, the resulting mixed oil and corn oil were uniformly melted and mixed in a mass ratio of 2:3 to obtain Oil 1, thereby lowering the melting point of the oil and facilitating its intake into the stomach.

[0146] Oil and Fat 2:OCFA algal oil (Yihai Kerry) and high-oleic sunflower seed oil (Yihai Kerry) were dissolved in a mass ratio of 1:0.1 and uniformly mixed. The resulting mixed oil and corn oil were uniformly melted and mixed in a mass ratio of 2:3 to obtain Oil and Fat 2. This lowered the melting point of the oil and fat. (In the animal experiments in this application, the oil and fat obtained by this preparation method were used.)

[0147] Oil 2 can also be prepared according to the following method: Glyceryl tritridecanoate, glyceryl tripentadecanoate, and glyceryl triheptadecanoate prepared according to the method described in Example 1, along with DHA algae oil (Qingdao Keyuan, obtained by refining purchased crude oil; for refining methods, see "Optimization of the refining processes for microalgae DHA" by Huang Huaixin; the crude oil batch is MKD120056) and high-oleic sunflower seed oil (Yihai Kerry, the same batch of product as the high-oleic sunflower seed oil used in Example 1), were melted and uniformly mixed in a mass ratio of 1:46:10:41:2. Then, the resulting mixed oil and corn oil were uniformly melted and mixed in a mass ratio of 2:3 to obtain oil 2, thereby lowering the melting point of the oil and facilitating its ingestion into the stomach.

[0148] 3. Fatty acid composition of oils and fats The fatty acid composition of fats 1 and 2 was measured using the third method, i.e., the "normalization method," as described in "GB5009.168-2016 Food Safety National Standard Determination of Fatty Acids in Foods." The results are shown in Table 33.

[0149] [Table 33]

[0150] 4. Animal experiments Experimental animals: Twenty-four pregnant female mice were selected for the experiment, and a 2x2 factorial design was used. On day 7.5 of gestation, the female mice were divided into four treatment groups, and each group underwent three replicate experiments (two female mice per replicate): (1) CON group, 2) OCFA group, 3) LP group, and 4) LP+OCFA group. Female mice in the CON and OCFA groups were given a normal diet with a protein content of 19% from day 7.5 of gestation, and intragastric administration of fat was performed once daily at a dose of 1 g / kg / day. The LP and LP+OCFA groups were given a low-protein diet with a protein level of 8%, and intragastric administration of fat was performed once daily at a dose of 1 g / kg / day. The daily feed amount and intragastric fat intake for each group are shown in Table 34. Female mice were fasted for 6 hours starting on day 18.5 of their gestation period, and then euthanized to collect samples for measurement and analysis. All relevant operating procedures met the requirements of the Animal Welfare and Animal Experiment Ethics Committee of China Agricultural University.

[0151] [Table 34]

[0152] 5.Results (1) Effects on glucose metabolism (improvement of insulin resistance) During pregnancy, the placenta produces many substances, including numerous hormones and cytokines. These substances can cause insulin resistance and affect the action of insulin. Insulin resistance becomes more pronounced in the second trimester, and many pregnant women may develop it during this period. The body can control blood sugar levels better by producing more insulin. However, in a small number of pregnant women, insulin production increases but not insufficient, ultimately leading to gestational diabetes. Pregnant women with gestational diabetes are more susceptible to complications such as fetal macrosomia, fetal malformations, premature birth, premature membrane rupture, and polyhydramnios. In severe cases, the fetal mortality rate may increase. Fasting serum glucose (GLU, mmol / L, measured using a biochemical analyzer), fasting insulin (INS, μIU / mL, ELISA assay), and fasting insulin resistance index (HOMA-IR = fasting serum blood glucose * fasting insulin / 22.5; for calculation method, see Linder, Katarzyna, et al. “Relationships of body composition and liver fat content with insulin resistance in obesity-matched estrogens and adults.” Obesity 22.5 (2014): 1325 to 1331) were measured. The results are shown in Table 35 and Figure 29. As can be seen from Figure 29, the insulin resistance index of pregnant mice in the OCFA group showed a decreasing trend compared to the CON group. Compared to the LP group, the insulin resistance index of pregnant mice in the LP+OCFA group was significantly reduced. The above results indicate that odd-carbon fatty acids are beneficial for controlling blood glucose levels during pregnancy by reducing insulin resistance during pregnancy. In particular, odd-carbon fatty acids are thought to be effective in improving insulin resistance caused by unhealthy diets (low-protein diets). Furthermore, odd-carbon fatty acids may also be effective in improving type 2 diabetes.

[0153] [Table 35]

[0154] (2) Influence on bile acid metabolism (decrease in serum bile acid level) Intrahepatic cholestasis of pregnancy is a pregnancy-specific disease, and the increase in serum bile acid level (TBA, measured using a biochemical analyzer) is a specific indicator. This complication may increase the risk of fetal distress, premature birth, and perinatal mortality. As can be seen from Table 36 and Figure 30, compared with the CON group, the serum bile acids of pregnant mice in the OCFA group were significantly decreased. As a result, it was shown that odd-chain fatty acids have the effect of decreasing serum bile acids in pregnant women. Compared with the CON group, the serum bile acid level of pregnant mice in the LP group was significantly increased, indicating that poor diet causes abnormal serum bile acids in pregnant mice and is not beneficial to fetal health. After supplementation with odd-chain fatty acids (LP + OCFA group), the serum bile acids of pregnant mice showed a decreasing trend. Generally, intrahepatic cholestasis of pregnancy is mainly treated by using hepatoprotective drugs. Therefore, those skilled in the art can predict that the combination of odd-chain fatty acids and hepatoprotective drugs should be effective in improving intrahepatic cholestasis of pregnancy caused by inappropriate diet or disease.

[0155]

Table 36

[0156] (3) Oxidative stress in the liver Superoxide dismutase (SOD) is the most important and optimal free radical scavenger in living organisms. Glutathione peroxidase (GSH-PX) is a widely present and important peroxide-degrading enzyme that reduces toxic peroxides to harmless hydroxyl compounds, preventing cell membrane structure and function from being disrupted or damaged by peroxides. Malondialdehyde (MDA) is a membrane lipid peroxidation product, and its amount directly reflects the level of peroxidation in the cell membrane. Excessive accumulation of malondialdehyde leads to cross-linking and polymerization of macromolecules in life, such as proteins and nucleic acids, resulting in changes in the structure and function of the cell membrane. Table 37 and Figure 31 show the effects of daily diet and fat administration on oxidative stress in the liver of pregnant mice. Figure 31 shows that, compared to the CON group, superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) levels were significantly increased and malondialdehyde (MDA) levels were significantly decreased in the livers of pregnant mice in the OCFA group. This indicates that odd-carbon fatty acids reduce oxidative stress in the livers of mammals that consume a normal diet during pregnancy and improve the body's antioxidant capacity. Compared to the CON group, superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) levels were significantly decreased and malondialdehyde (MDA) levels were significantly increased in the LP group, indicating that a low-protein diet caused oxidative stress in the livers of pregnant mice. However, compared to the LP group, liver superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) levels were significantly increased and malondialdehyde (MDA) levels were significantly decreased in the livers of pregnant mice in the LP+OCFA group. This indicates that odd-carbon fatty acids have the effect of reducing oxidative stress in pregnant mammals resulting from abnormal diets and improving the body's antioxidant capacity. All of the above results indicate that supplementation with odd-carbon fatty acids can reduce oxidative stress in the liver of pregnant mammals.

[0157] [Table 37]

[0158] (4) Colon health (I) Histological score The scoring method was as follows: The degree of epithelial cell damage, crypt damage, and inflammatory cell infiltration were observed under a microscope, and these three degrees were scored individually. The sum of the three scores was the final score. The results are shown in Table 38. For the evaluation method, we referred to Kim, Janice J., et al. “Investigating intestinal inflammation in DSS-induced model of IBD.” Journal of visualized experiments: JoVE 60 (2012).

[0159] Table 38 and Figure 32 show that the colon of the LP group showed significant structural changes, such as epithelial damage, compared to the CON group, while the colon of the LP+OCFA group showed repair of damage and approached the structure of the CON group. The significant increase in the histological score of the colon of pregnant mice in the LP group compared to the CON group indicates that the low-protein diet caused histopathological damage to the colon tissue. The significant decrease in the histological score of the colon of pregnant mice in the LP+OCFA group compared to the LP group indicates that odd-carbon fatty acids have an effect of improving histopathological damage to the intestinal tract caused by abnormal diet or disease.

[0160] [Table 38]

[0161] (ii) Inflammation of the intestinal tract Table 39 and Figure 33 show the effects of daily diet and oil treatment on the gene expression levels of five major inflammatory factors (IL-1β, IL-6, TNF-α, NLRP3, and GSDMD, as determined by quantitative PCR) in the colon of pregnant mice. As shown in Figure 33, in the normal diet group, dietary supplementation with odd-carbon fatty acids (OCFA group) reduced the expression levels of IL-1β and GSDMD in the colon tissue, suggesting that odd-carbon fatty acids can alleviate inflammation. Compared to the CON group, the group ingested a low-protein diet (LP group) showed a significant increase in the expression levels of the five inflammatory factors in the colon, suggesting that the low-protein diet exacerbated the inflammatory response in the colon. However, when mice fed a low-protein diet were supplemented with odd-carbon fatty acids (LP+OCFA group), the levels of all inflammatory factors decreased to or below the levels of the control group. This suggests that odd-carbon fatty acids may play a positive role in alleviating intestinal inflammation. Furthermore, the literature has reported that the high incidence of colorectal cancer is associated with some form of inflammation in the intestinal tract. Therefore, based on the above experimental results, those skilled in the art can predict that odd-carbon fatty acids may have beneficial effects on inflammatory bowel disease and colorectal cancer.

[0162] [Table 39]

[0163] (iii) Microecology of the intestinal tract Table 40 and Figure 34 show the effects of daily diet and oil treatment on two types of harmful bacteria in the intestinal tract of pregnant mice. Numerous studies have shown that Helicobacter pylori and Deferibacter can cause inflammation in the intestinal tract. Figure 34 shows that supplementing pregnant mice fed a normal diet with odd-carbon fatty acids (OCFA group) significantly reduced the abundance of Helicobacter pylori and Deferibacter microorganisms in their feces (fecal samples were collected from pregnant mice on the day of euthanasia, DNA was extracted, and 16S rRNA gene sequences were analyzed. DNA extraction and analysis were outsourced to Shanghai Majorbi.) In mice fed a low-protein diet, supplementation with odd-carbon fatty acids (LP+OCFA group) also reduced the abundance of Deferibacter microorganisms in the intestinal tract. This suggests that odd-carbon fatty acids may have an effect on improving the microbial ecosystem in the intestinal tract.

[0164] [Table 40]

[0165] Helicobacter pylori is a common human pathogen, infecting approximately half of the world's population. Helicobacter pylori infection can cause a range of gastrointestinal disorders of varying degrees, including chronic gastritis, indigestion, and peptic ulcers. Furthermore, Helicobacter pylori is clearly a human carcinogen and a significant cause of stomach cancer. Eradication therapy for Helicobacter pylori infection not only improves gastrointestinal disorders associated with the bacterium but can also effectively reduce the risk of developing stomach cancer.

[0166] Antibiotics are the current conventional method in the eradication therapy of Helicobacter pylori. However, the antibiotic resistance of Helicobacter pylori is gradually increasing worldwide, and the success rate of eradication therapy with antibiotics has been continuously decreasing. Furthermore, with the increase in research on the intestinal microbial ecology, the potential adverse effects of antibiotic treatment (especially the repeated use and long-term use of antibiotics) on the intestinal microbial ecology have also been widely noticed in the academic community. To address these existing problems and challenges, researchers have begun to search for other auxiliary and alternative treatment methods.

[0167] The results of the present invention suggest that odd-chain fatty acids may be used as an alternative or auxiliary method for the removal or treatment of Helicobacter pylori.

[0168] (5) Nutritional effect The ratio obtained by dividing the feed consumption by the weight gain is the feed-to-meat ratio, also known as the feed conversion rate. As can be seen from Table 41 and Figure 35, the feed conversion rate tended to increase in the OCFA group compared with the CON group. Also, the feed conversion rate tended to increase in the LP+OCFA group compared with the LP group. This indicates that odd-chain fatty acids are beneficial for weight management in pregnant mammals.

[0169] [Table 41]

[0170] Table 42 and Figure 36 show the effects of daily feed and fat administration on lipid metabolism in pregnant mice (measured using a blood biochemistry kit). Figure 36 shows that serum total cholesterol, triglycerides, HDL, and LDL were all significantly reduced in the low-LP group compared to the CON group, indicating that a low-protein diet caused abnormalities in the lipid metabolism of pregnant mice; however, the LP+OCFA group did not show a more pronounced reduction in the aforementioned indicators compared to the LP group, indicating that dietary supplementation with odd-carbon fatty acids does not adversely affect the lipid metabolism of pregnant mammals. Furthermore, the figure shows that serum high-density lipoprotein (HDL) was significantly increased in the OCFA group compared to the CON group, and significantly increased in the LP+OCFA group compared to the LP group. High-density lipoprotein is an anti-atherosclerotic plasma lipoprotein and a protective factor against coronary artery disease. The above results indicate that odd-carbon fatty acids can increase serum high-density lipoprotein, improve atherosclerosis, and reduce the risk of coronary artery disease.

[0171] [Table 42]

[0172] From the above description, it will be understood that while specific embodiments of the present invention have been described for illustrative purposes, the scope of the invention is not limited to these specific embodiments. Those skilled in the art can make various modifications or improvements to the invention without departing from the spirit and scope of the invention. All such modifications or improvements are within the scope of protection of the invention.

Claims

1. Use of odd-carbon fatty acids in the manufacture of formulations or pharmaceuticals for one or more of the following purposes: (1) Increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in the subject; in particular, increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in the intestinal tract (e.g., intestinal mucosa), more specifically, increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in the duodenum, jejunum, and ileum (e.g., their mucosa); (2) To reduce the amount of corticotropin-releasing hormone (CRF) in the target intestinal tissue; more preferably, to reduce the amount of corticotropin-releasing hormone (CRF) in the ileal tissue; (3) To improve or strengthen the mechanical barrier of the target intestinal tract; by improving the mechanical barrier of the intestinal tract, it is possible to prevent the invasion of bacteria, toxins, and foreign antigens into the body, maintain the stability of the internal environment, and prepare the foundation for nutrient absorption; (4) Increasing the content of immunoglobulins (e.g., IgG, IgA, and / or IgM) in the target intestinal tract; preferably increasing the content of immunoglobulins (e.g., 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; even more preferably increasing the content of immunoglobulin A in the ileum; (5) To increase the protein expression levels of TLR4 and NF-κB in the target intestinal tissue, particularly in the duodenum, jejunum, and ileum; (6) Maintaining homeostasis of ileal inflammatory cytokines (e.g., TNF-α, IL-1β, IL-6, and / or IL-10) in the subject; (7) To increase the expression level of ileal mucin 2 in the subject; (8) To increase the expression of HIF-1α in the intestinal tract and promote the survival of intestinal cells in a hypoxic environment within the intestinal tract; (9) Maintaining immune homeostasis in the target intestinal tract (especially the ileum); (10) To increase the content of nuclear protein Ki-67 in the target intestinal tissue, preferably the duodenum, jejunum and / or ileum; and to promote the proliferation of intestinal epithelial cells in the target; (11) Activating the mTOR signaling pathway in the target intestinal tract, increasing the expression level of activated mTOR protein in intestinal cells (particularly small intestinal cells such as the duodenum, jejunum, and ileum), and / or increasing the level of activated S6 kinase in intestinal cells (particularly small intestinal cells such as the duodenum, jejunum, and ileum); (12) To increase the levels of digestive enzymes (including but not limited to maltase, aminopeptidase and / or sucrase) in the target intestinal tract, particularly the small intestine, and to promote the absorption of nutrients; (13) To increase the 5-hydroxytryptamine content in the target intestinal tissue (especially the duodenum, jejunum, and / or ileum) and the substance P (neuropeptide) content in the ileum, thereby enhancing the function of the small intestine, such as by increasing intestinal peristalsis, promoting the contraction of gastrointestinal smooth muscle, suppressing the secretion of gastric acid and bile, and regulating local gastrointestinal blood flow; (14) To promote the development of the target intestinal tract; (15) Downregulating the expression levels of mitochondrial autophagy-related proteins (e.g., ULK1, TFEB, and / or parkin) in cells of the target intestinal tract (particularly the duodenum, jejunum, and / or ileum) to alleviate mitochondrial dysfunction; (16) Upregulating the levels of lipid synthesis-related transcription factors (such as PPARγ and / or SREBP-1) in the target intestinal tract (especially the small intestine, especially the duodenum and jejunum) to promote lipid absorption and assimilation in the intestinal tract (especially the small intestine); (17) To maintain energy homeostasis of target intestinal cells and improve energy metabolism in the intestines; (18) Upregulating the content of type I and type II muscle fibers and the expression level of mTOR protein in the target muscle tissue, while simultaneously decreasing the relative content of AMPK and PGC1-α; (19) To improve the energy state of the target 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; (20) To upregulate the expression level of SREBP-1 in the target muscle tissue, promote lipid anabolism, increase lipid uptake and utilization by muscle tissue, improve energy status, and promote muscle tissue development and metabolism; (21) To promote the development and metabolism of the target muscle tissue; (22) Upregulating the expression of activated mTOR in the target, decreasing the expression levels of Prdm16 and Irisin, inhibiting lipolysis, increasing lipid synthesis, and promoting the development of adipose tissue; (23) To upregulate the levels of SERBP-1 and APOB in the target adipose tissue, increase lipid synthesis in adipose tissue, promote lipid transport in the body, and maintain the energy balance between adipose tissue and the body; (24) To promote the development and metabolism of the target adipose tissue; (25) To upregulate the GSH-PX content in the target serum, improve the body's overall antioxidant capacity, and maintain overall redox equilibrium; (26) To reduce the levels of HIS, jejunal IgE, ileal IgE, jejunal HIS, and ileal HIS in the target blood, thereby reducing allergic reactions in the body and in the jejunum and ileum; (27) To reduce allergic reactions in the body and intestinal tract of the subject; (28) To reduce insulin resistance in pregnant subjects; (29) Controlling blood glucose levels in pregnant subjects; (30) Improving insulin resistance caused by an unhealthy diet (e.g., a low-protein diet); (31) To prevent gestational diabetes, and to prevent macrosomia, fetal malformations, premature birth, premature membrane rupture and / or polyhydramnios caused by gestational diabetes, and to reduce fetal mortality; (32) Lowering serum bile acid levels in pregnant subjects; (33) To prevent or improve pregnancy-related intrahepatic cholestasis (e.g., pregnancy-related intrahepatic cholestasis caused by inappropriate diet or disease) in the subjects; and to reduce the occurrence or risk of occurrence of fetal distress, premature birth, and perinatal mortality associated with pregnancy-related intrahepatic cholestasis in the subjects; (34) To increase the levels of superoxide dismutase and glutathione peroxidase in the liver of the subject, and to decrease the level of malondialdehyde in the liver of the subject, thereby reducing oxidative stress in the pregnant subject; (35) To improve the pathological damage to intestinal tissue caused by the abnormal diet or disease of the subject; (36) To reduce inflammatory bowel factors (e.g., IL-1β, IL-6, TNF-α, NLRP3, and / or GSDMD) in the subject and reduce inflammation of the intestinal tract; (37) To treat or prevent inflammatory bowel disease and colorectal cancer; (38) To reduce the amount of Helicobacter pylori and / or Deferibacter species in the subject's body and improve the microbial ecosystem in the intestinal tract; and (39) To prevent or treat diseases, including gastric cancer, caused by Helicobacter pylori bacteria in the subjects.

2. The use according to claim 1, comprising using odd-carbon fatty acids in the manufacture of formulations or pharmaceuticals for one or more of the following purposes: (1) Increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in the subject; in particular, increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in the intestinal tract (e.g., intestinal mucosa), more specifically, increasing the protein expression levels of tight junction-related proteins (e.g., occludin, claudin, and / or ZO-1) in the duodenum, jejunum, and ileum (e.g., their mucosa); and (2) Decreasing the content of corticotropin-releasing hormone (CRF) in the intestinal tissue of the subject; thereby improving or strengthening the mechanical barrier of the intestinal tract of the subject; and / or (4) Increasing the content of immunoglobulins (e.g., IgG, IgA, and / or IgM) in the target intestinal tract; preferably increasing the content of immunoglobulins (e.g., 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 even more preferably increasing the content of immunoglobulin A in the ileum; (5) In the target intestinal tissue, particularly the duodenum, jejunum, and ileum (6) To increase the protein expression levels of TLR4 and NF-κB in the subject; (7) To maintain homeostasis of ileal inflammatory cytokines (e.g., TNF-α, IL-1β, IL-6, and / or IL-10) in the subject; (8) To increase the expression level of ileal mucin 2 in the subject; and (9) To increase the expression of HIF-1α in the intestinal tract and promote the survival of intestinal cells under hypoxic conditions in the intestinal tract; thereby maintaining immune homeostasis in the subject's intestinal tract (especially the ileum); and / or (10) To increase the content of nuclear protein Ki-67 in the target intestinal tissue and promote the proliferation of target intestinal epithelial cells, the intestinal tissue is preferably the duodenum, jejunum and / or ileum; (11) To activate the mTOR signaling pathway in the target intestine, increase the expression level of activated mTOR protein in intestinal cells (especially small intestinal cells), and / or increase the level of activated S6 kinase in intestinal cells (especially small intestinal cells); (12) To increase the digestive enzyme (maltase) in the target intestine, especially the small intestine. (13) To increase the levels of aminopeptidase and / or sucrase (including but not limited to these) and promote the absorption of nutrients; and (13) To increase the 5-hydroxytryptamine content in the target intestinal tissue (particularly the duodenum, jejunum and / or ileum) and the substance P (neuropeptide) content in the ileum, thereby enhancing the function of the small intestine, such as by increasing intestinal peristalsis, promoting the contraction of gastrointestinal smooth muscle, suppressing gastric acid and bile secretion, and regulating local gastrointestinal blood flow; thereby promoting the development of the target intestinal tract; and / or (15) Downregulating the expression levels of mitochondrial autophagy-related proteins (e.g., ULK1, TFEB, and / or parkin) in target intestinal cells to alleviate mitochondrial dysfunction; and (16) Upregulating the levels of lipid synthesis-related transcription factors (e.g., PPARγ and / or SREBP-1) in target intestinal cells to promote lipid absorption and assimilation in the intestinal tract (especially the small intestine); thereby maintaining energy homeostasis of target intestinal cells and improving energy metabolism in the intestinal tract; and / or (18) Upregulating the content of type I and type II muscle fibers and the expression level of mTOR protein in the target muscle tissue, while simultaneously decreasing the relative content of AMPK and PGC1-α; (19) Improving the energy state of the target muscle tissue, promoting cell growth and tissue development, increasing the content of muscle fibers, 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 level of SREBP-1 in the target muscle tissue, promoting lipid anabolism, increasing lipid uptake and utilization by muscle tissue, improving the energy state, and promoting the development and metabolism of muscle tissue; thereby promoting the development and metabolism of the target muscle tissue; and / or (22) Upregulating the expression of activated mTOR in the target, decreasing the expression levels of Prdm16 and Irisin, inhibiting lipolysis, increasing lipid synthesis, and promoting the development of adipose tissue; and (23) Upregulating the levels of SERBP-1 and APOB in the target adipose tissue, increasing lipid synthesis in adipose tissue, promoting lipid transport in the body, and maintaining the energy balance between adipose tissue and the body; thereby promoting the development and metabolism of the target adipose tissue; and / or (25) Upregulating the GSH-PX content in the subject's serum to improve the body's overall antioxidant capacity and maintain overall redox equilibrium; and (26) Decreasing the content of HIS, jejunal IgE, ileal IgE, jejunal HIS, and ileal HIS in the subject's blood to reduce allergic reactions in the body and in the jejunum and ileum; thereby mitigating allergic reactions in the body and intestinal tract of the subject; and / or (28) to reduce insulin resistance in pregnant subjects; and (29) to control blood glucose levels in pregnant subjects; thereby preventing gestational diabetes, preventing macrosomia, fetal malformations, premature birth, premature membrane rupture and / or polyhydramnios caused by gestational diabetes, and / or reducing fetal mortality; and / or (32) to prevent or improve pregnancy-related intrahepatic cholestasis in pregnant subjects, such as pregnancy-related intrahepatic cholestasis caused by an inappropriate diet or disease, by lowering serum bile acid levels in pregnant subjects; and / or (33) to reduce the occurrence or risk of occurrence of fetal distress, preterm birth, and perinatal mortality associated with pregnancy-related intrahepatic cholestasis in subjects; and / or (34) to reduce oxidative stress in pregnant subjects by increasing the levels of superoxide dismutase and glutathione peroxidase in the liver of subjects and decreasing the levels of malondialdehyde in the liver of subjects; thereby (35) to improve the pathological damage effect on intestinal tissue caused by an abnormal diet or disease in subjects.

3. The use according to claim 1, comprising using odd-carbon fatty acids in the manufacture of formulations or pharmaceuticals for one or more of the following purposes: (3) to improve or strengthen the mechanical barrier of the target intestinal tract; (9) to maintain immune homeostasis in the target intestinal tract (especially the ileum); (14) to promote the development of the target intestinal tract; and (17) to maintain energy homeostasis of the cells of the target intestinal tract and improve energy metabolism in the intestinal tract; and / or (21) To promote the development and metabolism of the target muscle tissue; and / or (24) To promote the development and metabolism of the target adipose tissue; and / or (27) To reduce allergic reactions in the body and intestinal tract of the subject.

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

5. The odd-carbon fatty acid is used in the form of an oil containing the odd-carbon fatty acid; Preferably, in the fatty acid composition of the oil, the content of the odd-carbon fatty acids is ≥ 20%, for example, 20% to 70% or 20% to 60%; Preferably, in the fatty acid composition of the oil, the content of C11:0 fatty acids is 5% or less, preferably 1% or less, more preferably 0.5% or less; the content of C13:0 fatty acids is 1% to 5%, preferably 2% to 4%, and the content of C15:0 fatty acids is 15% to 70%, preferably 18% to 60%; the content of C17:0 fatty acids is 0.1% to 9%, and the content of C19:0 fatty acids is 5% or less, preferably 1% or less, even more preferably 0.5% or less; the content of C21:0 fatty acids is 5% or less, preferably 1% or less, even more preferably 0.5% or less; and the content of C23:0 fatty acids is 5% or less, preferably 1% or less, even more preferably 0.5% or less. The use described in claim 4.

6. The fatty acid composition of the oil is 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 The use according to claim 5, further comprising one or more of C16:5, C22:6, C24:0 and C24:1; preferably, in the fatty acid composition of the oil, the content of C16:0 is 2% to 15%, for example 4% to 13%; the content of C18:0 is ≤5%, for example 0% to 5% or 0% to 3%; the content of C18:1 is 5% to 35%, for example 7% to 33%; the content of C18:2 is ≤35%, for example 0% to 35%; the content of C22:5 is ≤5%, for example 0% to 5% or 1% to 3.5%; the content of C22:6 is 5% to 25%, for example 8% to 22%; and the content of the remaining fatty acids is 1% or less or less than 0.5%.

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

8. The aforementioned oils and fats are derived from edible oils, their transesterification products, or combinations thereof; Preferably, the edible oil is selected from vegetable oil, microbial oil, animal oil, or any combination thereof; The aforementioned vegetable oils include one or more of the following: 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, Triadica cevifera seed oil, sweet almond oil, almond oil, Vernicia fordii 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, cocoa butter, or fractions thereof, their transesterification products, or transesterification products of two or more oils and fats; Preferably, the animal oil is selected from one or more of lard, chicken fat, mutton fat, fish oil, and beef fat; Preferably, the microbial oil comprises lipids derived from microorganisms selected from the following groups: algae, e.g., Traustochytriales (more specifically, including strains of the genera Traustochytrium and Schizochytrium); oily bacteria, e.g., Rhodococcus (e.g., Rhodococcus opacus); oily yeasts, e.g., Yarovia (e.g., Yarovia liporitica); mutant strains and mixed strains thereof derived from any of the above strains, the microorganism is preferably of the genus Schizochytrium; and Preferably, the weight ratio of the transesterified odd-carbon fatty acid triglyceride to the vegetable oil is 45-70:30-55, 50-65:35-50, or 55-62:38-45. The use described in any one of claims 5 to 7.

9. The oil is a chemical transesterification product of an odd-carbon fatty acid-containing triglyceride, DHA algae oil, and high-oleic sunflower seed oil; preferably, in a mixture of the odd-carbon fatty acid-containing triglyceride, DHA algae oil, and high-oleic sunflower seed oil, the weight ratio of triglyceride pentadecanoic acid, DHA algae oil, and high-oleic sunflower seed oil is 40-50:30-45:1-10, for example, 40-50:30-40:5-10 or 40-50:38-45:1-5; preferably, in the fatty acid composition of the oil, the C15:0 content is The C16:0 content is 12% to 25%, preferably 16% to 22%, the C16:0 content is 5% to 15%, preferably 10% to 15%, the C17:0 content is 1% to 7%, preferably 2% to 5%, the C18:0 content is 0.5% to 3%, preferably 1% to 2%, the C18:1 content is 12% to 22%, preferably 15% to 20%, the C18:2 content is 25% to 35%, preferably 30% to 35%, and the C22:6 content is 5% to 15%, preferably 7% to 12%; the content of the remaining fatty acids is usually less than 1% or less than 0.5%; or The oil is a chemical transesterification product of an odd-carbon fatty acid-containing triglyceride, palm stearin, and high-oleic sunflower seed oil; preferably, in a mixture of the odd-carbon fatty acid-containing triglyceride, palm stearin, and high-oleic sunflower seed oil, the weight ratio of pentadecanoic acid triglyceride to palm stearin and high-oleic sunflower seed oil is 55-62:1-5:35-40; in the fatty acid composition of the oil, C The content of C15:0 is 40% to 65%, preferably 50% to 60%, the content of C16:0 is 1% to 7%, preferably 3% to 5.5%, the content of C17:0 is 0.1% to 3%, preferably 0.1% to 1%, the content of C18:0 is 1% to 5%, preferably 1% to 3%, the content of C18:1 is 25% to 35%, preferably 28% to 34%, and the content of C18:2 is 1% to 5%, preferably 2% to 4%; the content of the remaining fatty acids is usually less than 1% or less than 0.5%. The use described in claim 8.

10. The oil and fat according to any one of claims 4 to 9.

11. A formulation comprising an odd-carbon fatty acid or oil / fat according to any one of claims 1 to 9; preferably, the formulation is a nutritional supplement.

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