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Adipose tissue deletion of Gpr116 impairs insulin sensitivity through modulation of adipose function
Author(s) -
Nie Tao,
Hui Xiaoyan,
Gao Xuefei,
Li Kuai,
Lin Wanhua,
Xiang Xiaoliang,
Ding Mengxiao,
Kuang Ying,
Xu Aimin,
Fei Jian,
Wang Zhugang,
Wu Donghai
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.08.006
Subject(s) - adipose tissue , resistin , medicine , endocrinology , adiponectin , insulin resistance , adipocyte , receptor , conditional gene knockout , energy homeostasis , in vivo , homeostasis , biology , knockout mouse , chemistry , insulin , phenotype , biochemistry , gene , microbiology and biotechnology
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.