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二氢杨梅素通过调节肠道微生物群-鹅去氧胆酸途径促进胰高血糖素样肽-1分泌并改善胰岛素抵抗。

Dihydromyricetin Promotes Glucagon-Like Peptide-1 Secretion and Improves Insulin Resistance by Modulation of the Gut Microbiota-CDCA Pathway.

作者信息

Li Pengfei, Zhang Yong, Lang Hedong, Hou Pengfei, Yao Yu, Zhang Ruiliang, Wang Xiaolan, Zhang Qianyong, Mi Mantian, Yi Long

机构信息

Research Center for Nutrition and Food Safety, Chongqing Key Laboratory of Nutrition and Health, Chongqing Medical Nutrition Research Center, Institute of Military Preventive Medicine, Third Military Medical University, Chongqing, P.R. China.

出版信息

Mol Nutr Food Res. 2025 Apr;69(8):e202400491. doi: 10.1002/mnfr.202400491. Epub 2025 Mar 13.

DOI:10.1002/mnfr.202400491
PMID:40078029
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12020986/
Abstract

Insulin resistance is a common metabolic disease, and its pathogenesis is still unclear. The decrease of glucagon-like peptide-1 (GLP-1) level mediated by the alteration of gut microbiota may be the pathogenesis. The study was to investigate the regulatory effect of dihydromyricetin (DHM) on GLP-1 level and insulin resistance induced by high-fat diet (HFD), and to further explore its possible molecular mechanism. Mice were fed an HFD to establish the model of insulin resistance to determine whether DHM had a protective effect. DHM could improve insulin resistance. DHM increased serum GLP-1 by improving intestinal GLP-1 secretion and inhibiting GLP-1 decomposition, associated with the alteration of intestinal intraepithelial lymphocytes (IELs) proportions and decreased expression of CD26 in IELs and TCRαβ CD8αβ IELs in HFD-induced mice. DHM could ameliorate GLP-1 level and insulin resistance by modulation of gut microbiota and the metabolites, particularly the regulation of chenodeoxycholic acid (CDCA) content, followed by the inhibition of farnesoid X receptor (FXR) expression in intestinal L cells and increased glucagon gene (Gcg) mRNA expression and GLP-1 secretion. This research demonstrates the role of "gut microbiota-CDCA" pathway in the improvement of intestinal GLP-1 levels in HFD-induced mice by DHM administration, providing a new target for the prevention of insulin resistance.

摘要

胰岛素抵抗是一种常见的代谢性疾病，其发病机制仍不清楚。由肠道微生物群改变介导的胰高血糖素样肽-1（GLP-1）水平降低可能是其发病机制。本研究旨在探讨二氢杨梅素（DHM）对高脂饮食（HFD）诱导的GLP-1水平和胰岛素抵抗的调节作用，并进一步探索其可能的分子机制。给小鼠喂食高脂饮食以建立胰岛素抵抗模型，以确定DHM是否具有保护作用。DHM可改善胰岛素抵抗。DHM通过改善肠道GLP-1分泌和抑制GLP-1分解来增加血清GLP-1，这与高脂饮食诱导的小鼠肠道上皮内淋巴细胞（IELs）比例的改变以及IELs、TCRαβ CD8αβ IELs中CD26表达降低有关。DHM可通过调节肠道微生物群及其代谢产物，特别是调节鹅去氧胆酸（CDCA）含量，进而抑制肠道L细胞中法尼醇X受体（FXR）的表达，增加胰高血糖素基因（Gcg）mRNA表达和GLP-1分泌，从而改善GLP-1水平和胰岛素抵抗。本研究证明了“肠道微生物群-CDCA”途径在通过给予DHM改善高脂饮食诱导的小鼠肠道GLP-1水平中的作用，为预防胰岛素抵抗提供了新的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/eb5e68290212/MNFR-69-e202400491-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/01164bf88bfc/MNFR-69-e202400491-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/e5ca26396963/MNFR-69-e202400491-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/96d8544ca699/MNFR-69-e202400491-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/ad13e6337067/MNFR-69-e202400491-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/dedf3779ea29/MNFR-69-e202400491-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/eb5e68290212/MNFR-69-e202400491-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/01164bf88bfc/MNFR-69-e202400491-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/eb2eb43ef551/MNFR-69-e202400491-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/f26710c3e87f/MNFR-69-e202400491-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/00a04dce42b3/MNFR-69-e202400491-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/e5ca26396963/MNFR-69-e202400491-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/96d8544ca699/MNFR-69-e202400491-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/ad13e6337067/MNFR-69-e202400491-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/dedf3779ea29/MNFR-69-e202400491-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21b3/12020986/eb5e68290212/MNFR-69-e202400491-g006.jpg

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Dihydromyricetin supplementation improves ethanol-induced lipid accumulation and inflammation.补充二氢杨梅素可改善乙醇诱导的脂质积累和炎症。
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