GPR10 deficiency in mice results in altered energy expenditure and obesity
GPR10 deficiency in mice results in altered energy expenditure and obesity
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DOI：
10.1016/j.bbrc.2007.09.016
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发表时间：
2007-11-23
影响因子：
3.1
通讯作者：
Bohlooly-Y, Mohammad
中科院分区：
文献类型：
--
作者：
Bjursell, Mikael;Lenneras, Maria;Bohlooly-Y, Mohammad
在这项研究中，我们研究了携带GPR 10 （GPR 10 KO）基因的小鼠，以阐明该受体在代谢中的功能和重要性。雌性和雄性GPR 10 KO小鼠分别在I和15周龄后体重增加。体重的增加是脂肪量增加的结果。肥胖在雌性小鼠中更为明显，它们的能量消耗也显著减少。与肥胖相关的是，与WT小鼠相比，在GPR10 KO中发现了更高的血浆瘦素水平、总胆固醇以及LDL和HDL的部分。有趣的是，GPR10 KO雌性小鼠的相对食物摄入量减少与下丘脑厌食信号CRH和POMC的高表达水平相关。综上所述，缺乏编码GPR10基因的雌性小鼠由于能量消耗较低而导致体重增加和肥胖。(C) 2007爱思唯尔公司版权所有。
In this study, mice carrying a disrupted gene encoding GPR 10 (GPR 10 KO) were studied to elucidate the function and importance of this receptor regarding metabolism. Female and male GPR 10 KO mice had higher body weight after I I 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. (C) 2007 Elsevier Inc. All rights reserved.