Bjursell Mikael, Lennerås Maria, Göransson Melker, Elmgren Anders, Bohlooly-Y Mohammad
Astrazeneca R&D Mölndal, S-43183 Mölndal, Sweden.
Biochem Biophys Res Commun. 2007 Nov 23;363(3):633-8. doi: 10.1016/j.bbrc.2007.09.016. Epub 2007 Sep 18.
In this study, mice carrying a disrupted gene encoding GPR10 (GPR10 KO) were studied to elucidate the function and importance of this receptor regarding metabolism. Female and male GPR10 KO mice had higher body weight after 11 and 15 weeks of age, respectively. The increased body weight was a result of increased fat mass. The obesity was much more pronounced in female mice, which also had a significant decrease in energy expenditure. In correlation to obesity, higher plasma levels of leptin, total cholesterol, and fractions of LDL and HDL were found in GPR10 KO compared to WT mice. Interestingly, GPR10 KO female mice had decreased relative food intake in correlation to higher hypothalamic expression levels of the anorexic signals CRH and POMC. In conclusion, female mice deficient of the gene encoding GPR10 develop higher body weight and obesity due to lower energy expenditure.
在本研究中,对携带编码GPR10的基因被破坏的小鼠(GPR10基因敲除小鼠)进行了研究,以阐明该受体在代谢方面的功能和重要性。雌性和雄性GPR10基因敲除小鼠分别在11周龄和15周龄后体重增加。体重增加是脂肪量增加的结果。肥胖在雌性小鼠中更为明显,其能量消耗也显著降低。与肥胖相关,与野生型小鼠相比,GPR10基因敲除小鼠的血浆瘦素、总胆固醇以及低密度脂蛋白和高密度脂蛋白组分水平更高。有趣的是,GPR10基因敲除雌性小鼠的相对食物摄入量减少,同时厌食信号CRH和POMC在下丘脑的表达水平升高。总之,缺乏编码GPR10基因的雌性小鼠由于能量消耗降低而体重增加并出现肥胖。