胰岛素抵抗
胰高血糖素样肽-1
内分泌学
肠道菌群
内科学
胰岛素
胰高血糖素样肽-2
生物
2型糖尿病
化学
糖尿病
免疫学
医学
生物化学
肽
作者
Pengfei Li,Yong Zhang,Hedong Lang,Pengfei Hou,Yu Yao,Ruiliang Zhang,Xiaolan Wang,Qianyong Zhang,Mantian Mi,Yi Long
标识
DOI:10.1002/mnfr.202400491
摘要
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.
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