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Publication : Adipose tissue deletion of Gpr116 impairs insulin sensitivity through modulation of adipose function.

First Author  Nie T Year  2012
Journal  FEBS Lett Volume  586
Issue  20 Pages  3618-25
PubMed ID  22971422 Mgi Jnum  J:190131
Mgi Id  MGI:5448109 Doi  10.1016/j.febslet.2012.08.006
Citation  Nie T, et al. (2012) Adipose tissue deletion of Gpr116 impairs insulin sensitivity through modulation of adipose function. FEBS Lett 586(20):3618-25
abstractText  G protein-coupled receptor 116 (GPR116) is a novel member of the G protein-coupled receptors and its function is largely unknown. To investigate the physiological function of GPR116 in vivo, we generated adipose tissue specific conditional Gpr116 knockout mice (CKO) and fed them on standard chow or high fat diets. Selective deletion of Gpr116 in adipose tissue caused a pronounced glucose intolerance and insulin resistance in mice, especially when challenged with a high fat diet. Biochemical analysis revealed a more severe hepatosteatosis in CKO mice. Additionally, we found that CKO mice showed a lowered concentration of circulating adiponectin and an increased level of serum resistin. Our study suggests that GPR116 may play a critical role in controlling adipocyte biology and systemic energy homeostasis.
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