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肠道微生物群与胰高血糖素样肽-1

Gut microbiota and GLP-1.

作者信息

Everard Amandine, Cani Patrice D

机构信息

WELBIO (Walloon Excellence in Life sciences and BIOtechnology), Metabolism and Nutrition research group, Université catholique de Louvain, Louvain Drug Research Institute, Av. E. Mounier, 73, Box B1.73.11, 1200, Brussels, Belgium.

出版信息

Rev Endocr Metab Disord. 2014 Sep;15(3):189-96. doi: 10.1007/s11154-014-9288-6.

Abstract

A large body of evidence suggests that the regulation of energy balance and glucose homeostasis by fermentable carbohydrates induces specific changes in the gut microbiota. Among the mechanisms, our research group and others have demonstrated that the gut microbiota fermentation (i.e., bacterial digestion of specific compounds) of specific prebiotics or other non-digestible carbohydrates is associated with the secretion of enteroendocrine peptides, such as the glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), produced by L-cells. In this review, we highlight past and recent results describing how dietary manipulation of the gut microbiota, using nutrients or specific microbes, can stimulate GLP-1 secretion in rodents and humans. Furthermore, the purpose of this review is to discuss the putative mechanisms by which specific bacterial metabolites, such as short chain fatty acids, trigger GLP-1 secretion through GPR41/43-dependent mechanisms. Moreover, we conclude by discussing the molecular advance showing that the endocannabinoid system or related bioactive lipids modulated by the gut microbiota may contribute to the regulation of glucose, lipid and energy homeostasis.

摘要

大量证据表明,可发酵碳水化合物对能量平衡和葡萄糖稳态的调节会引起肠道微生物群的特定变化。在这些机制中,我们的研究小组和其他团队已经证明,特定益生元或其他不可消化碳水化合物的肠道微生物群发酵(即特定化合物的细菌消化)与肠内分泌肽的分泌有关,如L细胞产生的胰高血糖素样肽-1(GLP-1)和肽YY(PYY)。在这篇综述中,我们重点介绍过去和最近的研究结果,这些结果描述了利用营养素或特定微生物对肠道微生物群进行饮食调控如何刺激啮齿动物和人类的GLP-1分泌。此外,本综述的目的是讨论特定细菌代谢产物(如短链脂肪酸)通过GPR41/43依赖性机制触发GLP-1分泌的假定机制。此外,我们通过讨论分子进展得出结论,即肠道微生物群调节的内源性大麻素系统或相关生物活性脂质可能有助于调节葡萄糖、脂质和能量稳态。

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