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G(s)alpha deficiency in adipose tissue leads to a lean phenotype with divergent effects on cold tolerance and diet-induced thermogenesis.

Authors: Chen, Min  Chen, Hui  Nguyen, Annie  Gupta, Divakar  Wang, Jie  Lai, Edwin W  Pacak, Karel  Gavrilova, Oksana  Quon, Michael J  Weinstein, Lee S 
Citation: Chen M, etal., Cell Metab. 2010 Apr 7;11(4):320-30. doi: 10.1016/j.cmet.2010.02.013.
Pubmed: (View Article at PubMed) PMID:20374964
DOI: Full-text: DOI:10.1016/j.cmet.2010.02.013

G(s)alpha, the G protein that mediates receptor-stimulated cAMP generation, has been implicated as a regulator of adipogenesis and adipose tissue function. Heterozygous G(s)alpha mutations lead to obesity in Albright hereditary osteodystrophy (AHO) patients and in mice. In this study, we generated mice with adipose-specific G(s)alpha deficiency. Heterozygotes had 50% loss of G(s)alpha expression in adipose tissue and no obvious phenotype, suggesting that adipose-specific G(s)alpha deficiency is not the cause of obesity in AHO. Homozygotes (FGsKO) had severely reduced adipose tissue, indicating that G(s)alpha is required for adipogenesis. Although FGsKO mice had impaired cold tolerance and reduced responsiveness of brown adipose tissue (BAT) to sympathetic signaling, diet-induced thermogenesis and fatty acid oxidation in skeletal muscle were increased. In normal mice, high-fat diet raised sympathetic nerve activity in muscle, but not in BAT. Our results show that cold- and diet-induced thermogenesis may occur in separate tissues, especially when BAT function is impaired.


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RGD Object Information
RGD ID: 13673768
Created: 2018-06-23
Species: All species
Last Modified: 2018-06-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.