肠道菌群
串扰
胰高血糖素样肽-2
肠道通透性
G蛋白偶联胆汁酸受体
肠促胰岛素
胰高血糖素样肽-1
2型糖尿病
法尼甾体X受体
生物
胆汁酸
糖尿病
内分泌学
免疫学
生物化学
肽
物理
光学
基因
转录因子
核受体
作者
Yuan Zeng,Yifan Wu,Qian Zhang,Xinhua Xiao
出处
期刊:MBio
[American Society for Microbiology]
日期:2023-12-06
卷期号:15 (1)
被引量:54
标识
DOI:10.1128/mbio.02032-23
摘要
Gut microbiota exert influence on gastrointestinal mucosal permeability, bile acid metabolism, short-chain fatty acid synthesis, dietary fiber fermentation, and farnesoid X receptor/Takeda G protein-coupled receptor 5 (TGR5) signal transduction. The incretin glucagon-like peptide 1 (GLP-1) is mainly produced by L cells in the gut and regulates postprandial blood glucose. Changes in gut microbiota composition and function have been observed in obesity and type 2 diabetes (T2D). Meanwhile, the function and rhythm of GLP-1 have also been affected in subjects with obesity or T2D. Therefore, it is necessary to discuss the link between the gut microbiome and GLP-1. In this review, we describe the interaction between GLP-1 and the gut microbiota in metabolic diseases. On the one hand, gut microbiota metabolites stimulate GLP-1 secretion, and gut microbiota affect GLP-1 function and rhythm. On the other hand, the mechanism of action of GLP-1 on gut microbiota involves the inflammatory response. Additionally, we discuss the effects and mechanism of various interventions, such as prebiotics, probiotics, antidiabetic drugs, and bariatric surgery, on the crosstalk between gut microbiota and GLP-1. Finally, we stress that gut microbiota can be used as a target for metabolic diseases, and the clinical application of GLP-1 receptor agonists should be individualized.
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