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TGR5-mediated bile acid sensing controls glucose homeostasis.

Cell metabolism | 2009

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 in vivo, 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 in vivo, and suggest that pharmacological targeting of TGR5 may constitute a promising incretin-based strategy for the treatment of diabesity and associated metabolic disorders.

Pubmed ID: 19723493 RIS Download

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Associated grants

  • Agency: NIDDK NIH HHS, United States
    Id: P01 DK059820
  • Agency: NIDDK NIH HHS, United States
    Id: P01 DK059820-080006
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK067320
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK067320-04

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