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Mice lacking GPR3 receptors display late-onset obese phenotype due to impaired thermogenic function in brown adipose tissue.

Authors: Godlewski, G  Jourdan, T  Szanda, G  Tam, J  Cinar, R  Harvey-White, J  Liu, J  Mukhopadhyay, B  Pacher, P  Ming Mo, F  Osei-Hyiaman, D  Kunos, G 
Citation: Godlewski G, etal., Sci Rep. 2015 Oct 12;5:14953. doi: 10.1038/srep14953.
Pubmed: (View Article at PubMed) PMID:26455425
DOI: Full-text: DOI:10.1038/srep14953

We report an unexpected link between aging, thermogenesis and weight gain via the orphan G protein-coupled receptor GPR3. Mice lacking GPR3 and maintained on normal chow had similar body weights during their first 5 months of life, but gained considerably more weight thereafter and displayed reduced total energy expenditure and lower core body temperature. By the age of 5 months GPR3 KO mice already had lower thermogenic gene expression and uncoupling protein 1 protein level and showed impaired glucose uptake into interscapular brown adipose tissue (iBAT) relative to WT littermates. These molecular deviations in iBAT of GPR3 KO mice preceded measurable differences in body weight and core body temperature at ambient conditions, but were coupled to a failure to maintain thermal homeostasis during acute cold challenge. At the same time, the same cold challenge caused a 17-fold increase in Gpr3 expression in iBAT of WT mice. Thus, GPR3 appears to have a key role in the thermogenic response of iBAT and may represent a new therapeutic target in age-related obesity.


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RGD Object Information
RGD ID: 11531556
Created: 2016-09-02
Species: All species
Last Modified: 2016-09-02
Status: ACTIVE


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