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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。

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

机构信息

Key Laboratory of Regenerative Biology, Guangzhou Institute of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.

出版信息

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.

摘要

G 蛋白偶联受体 116(GPR116)是 G 蛋白偶联受体的一个新成员,其功能在很大程度上尚不清楚。为了研究 GPR116 在体内的生理功能,我们生成了脂肪组织特异性条件性 Gpr116 敲除小鼠(CKO),并让它们食用标准饲料或高脂肪饮食。选择性地在脂肪组织中敲除 Gpr116 会导致小鼠明显的葡萄糖不耐受和胰岛素抵抗,尤其是在高脂肪饮食的挑战下。生化分析显示 CKO 小鼠的肝脂肪变性更为严重。此外,我们发现 CKO 小鼠的循环脂联素浓度降低,血清抵抗素水平升高。我们的研究表明,GPR116 可能在控制脂肪细胞生物学和全身能量平衡方面发挥关键作用。

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