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

FEBS Lett. 2012 Oct 19;586(20):3618-25. doi: 10.1016/j.febslet.2012.08.006. Epub 2012 Aug 14.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes / metabolism
  • Adipocytes / pathology
  • Adipokines / metabolism
  • Adipose Tissue / metabolism*
  • Adipose Tissue / pathology*
  • Animals
  • Cell Differentiation / genetics
  • Cell Size
  • Gene Expression Regulation / genetics
  • Gene Knockout Techniques
  • Glucose Intolerance / genetics
  • Hyperlipidemias / genetics
  • Hyperlipidemias / metabolism
  • Hyperlipidemias / pathology
  • Insulin Resistance / genetics*
  • Lipid Metabolism / genetics
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Receptors, G-Protein-Coupled / deficiency*
  • Receptors, G-Protein-Coupled / genetics*

Substances

  • Adipokines
  • Gpr116 protein, mouse
  • Receptors, G-Protein-Coupled