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肠道菌群失调对胰高血糖素样肽-1 敏感性的调节。

Regulation of glucagon-like peptide-1 sensitivity by gut microbiota dysbiosis.

机构信息

Department of Diabetes, Endocrinology and Nutrition, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

出版信息

J Diabetes Investig. 2018 Mar;9(2):262-264. doi: 10.1111/jdi.12762. Epub 2017 Dec 1.

DOI:10.1111/jdi.12762
PMID:29034596
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5835457/
Abstract

Gut microbiota dysbiosis reduces expression of GLP-1 receptor (GLP-1R) and neuronal nitric oxide synthase (nNOS) in the enteric nervous system and hampers GLP-1-induced nitric oxide (NO) production through a pattern recognition receptor (PRR)-dependent mechanism, hence preventing activation of the gut-brain-periphery axis for control of insulin secretion and gastric emptying.

摘要

肠道微生物群落失调会降低肠神经系统中胰高血糖素样肽-1 受体 (GLP-1R) 和神经元型一氧化氮合酶 (nNOS) 的表达，并通过模式识别受体 (PRR) 依赖的机制阻碍 GLP-1 诱导的一氧化氮 (NO) 产生，从而防止肠道-脑-外周轴的激活以控制胰岛素分泌和胃排空。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23fa/5835457/530d903dab72/JDI-9-262-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23fa/5835457/530d903dab72/JDI-9-262-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23fa/5835457/530d903dab72/JDI-9-262-g001.jpg

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