Adipose tissue deletion of Gpr116 impairs insulin sensitivity through modulation of adipose function
Adipose tissue deletion of Gpr116 impairs insulin sensitivity through modulation of adipose function
复制标题
脂肪组织中 Gpr116 的缺失通过调节脂肪功能损害胰岛素敏感性
DOI：
10.1016/j.febslet.2012.08.006
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发表时间：
2012-10-19
期刊：
影响因子：
3.5
通讯作者：
Wu, Donghai
中科院分区：
文献类型：
--
作者：
Nie, Tao;Hui, Xiaoyan;Wu, Donghai
G蛋白偶联受体116（GPR116）是G蛋白偶联受体的新成员，其功能尚不清楚。为了研究GPR116在体内的生理功能，我们产生了脂肪组织特异性条件性Gpr116敲除小鼠（CKO），并以标准食物或高脂肪饮食喂养它们。脂肪组织中Gpr116的选择性缺失导致小鼠明显的葡萄糖耐受不良和胰岛素抵抗，特别是当用高脂肪饮食进行挑战时。生化分析显示CKO小鼠的肝脂肪变性更严重。此外，我们发现CKO小鼠循环脂联素浓度降低，血清脂联素水平升高。我们的研究表明，GPR116可能在控制脂肪细胞生物学和系统能量稳态方面发挥关键作用。(C)2012年欧洲生物化学学会联合会。Elsevier B.V.出版，保留所有权利。
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. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.