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A new life for bile acids.

Abstract：

:TGR5 is a G protein-coupled receptor expressed in brown adipose tissue and muscle, where its activation by bile acids triggers an increase in energy expenditure and attenuates diet-induced obesity. Using a combination of pharmacological and genetic gain- and loss-of-function studies invivo, we show here that TGR5 signaling induces intestinal glucagon-like peptide-1 (GLP-1) release, leading to improved liver and pancreatic function and enhanced glucose tolerance in obese mice. In addition, we show that the induction of GLP-1 release in enteroendocrine cells by 6alpha-ethyl-23(S)-methyl-cholic acid (EMCA, INT-777), a specific TGR5 agonist, is linked to an increase of the intracellular ATP/ADP ratio and a subsequent rise in intracellular calcium mobilization. Altogether, these data show that the TGR5 signaling pathway is critical in regulating intestinal GLP-1 secretion invivo, and suggest that pharmacological targeting of TGR5 may constitute a promising incretin-based strategy for the treatment of diabesity and associated metabolic disorders.

journal_name

J Hepatol

journal_title

Journal of hepatology

authors

Jansen PL

doi

10.1016/j.jhep.2010.02.003

subject

Has Abstract

pub_date

2010-06-01 00:00:00

pages

937-8

issue

6

eissn

0168-8278

issn

1600-0641

pii

S0168-8278(10)00099-1

journal_volume

52

pub_type

评论,杂志文章

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