LRH-1 heterozygous knockout mice are prone to mild obesity
LRH-1 heterozygous knockout mice are prone to mild obesity
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DOI：
10.1507/endocrj.ej14-0017
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发表时间：
2014-05-20
影响因子：
2
通讯作者：
Takeda, Jun
中科院分区：
文献类型：
--
作者：
Hattori, Taisuke;Iizuka, Katsumi;Takeda, Jun
肥胖是一个全球性的健康问题，它会增加患几种常见疾病的风险。肝脏受体同源物-1 （LRH-1）在类固醇激素代谢中起重要作用，影响体重。LRH-1基因缺失是否导致肥胖尚不清楚。本研究利用LRH-1杂合敲除（LRH-1(+/-)）小鼠，研究了LRH-1对体重增加和糖脂代谢的作用。LRH-1（+/-）小鼠在喂食高脂肪食物后，与野生型同窝小鼠相比，体重有轻微但显著的增加。我们进行了葡萄糖耐量试验和胰岛素耐量试验，未发现野生型和LRH-1（+/-）小鼠之间有任何显著差异。为了阐明LRH-1基因缺失如何影响体重增加，我们测量了食物摄入量、耗氧量、呼吸商、自发活动和直肠温度，并发现野生型和LRH-1（+/-）小鼠在喂食正常饮食和高脂肪饮食之间没有显著差异。结果表明，LRH-1杂合基因缺失导致体重增加，但糖脂代谢没有明显恶化。确定LRH-1对体重的影响将有助于了解肥胖的发病机制。
Obesity is a global health problem that increases the risk of several common diseases. Liver receptor homologue-1 (LRH-1) has an important role in steroid hormone metabolism, which influences body weight. Whether LRH-1 gene deletion causes obesity is yet to be clarified. In this study using LRH-1 heterozygous knockout (LRH-1(+/-)) mice, we investigated the role of LRH-1 on body weight gain and glucose and lipid metabolism. LRH-1(+/-) mice showed mild but significant body weight gains compared with wild-type littermate mice after being fed a high-fat diet. We performed glucose tolerance tests and insulin tolerance tests and did not find any significant differences between wild-type and LRH-1(+/-) mice. To clarify how LRH-1 gene deletion affects body weight gain, we measured food intake, oxygen consumption, respiratory quotient, spontaneous activity and rectal temperature, and found no significant differences between wild-type and LRH-1(+/-) mice fed a normal diet and a high-fat diet. The results suggest that heterozygous gene deletion of LRH-1 causes body weight gains without any apparent worsening of glucose and lipid metabolism. Identifying the effects of LRH-1 on body weight will aid in understanding the pathogenesis of obesity.