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Mex3c 突变部分通过增加体力活动减少肥胖。

Mex3c mutation reduces adiposity partially through increasing physical activity.

机构信息

Institute for Regenerative MedicineWake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USADepartment of Human Anatomy and EmbryologyThe Second Military Medical University, Shanghai 200433, ChinaInstitute for Regenerative MedicineWake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USADepartment of Human Anatomy and EmbryologyThe Second Military Medical University, Shanghai 200433, China.

Institute for Regenerative MedicineWake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USADepartment of Human Anatomy and EmbryologyThe Second Military Medical University, Shanghai 200433, China.

出版信息

J Endocrinol. 2014 Jun;221(3):457-68. doi: 10.1530/JOE-14-0071. Epub 2014 Apr 16.

DOI:10.1530/JOE-14-0071
PMID:24741071
Abstract

MEX3C is an RNA-binding protein with unknown physiological function. We have recently reported that a Mex3c mutation in mice causes growth retardation and reduced adiposity, but how adiposity is reduced remains unclear. Herein, we show that homozygous Mex3c gene trap mice have increased physical activity. The Mex3c mutation consistently conferred full protection from diet-induced obesity, hyperglycemia, insulin resistance, hyperlipidemia, and hepatic steatosis. In ob/ob mice with leptin deficiency, the Mex3c mutation also increased physical activity and improved glucose and lipid profiles. Expressing cre in the neurons of Mex3c gene trap mice, an attempt to partially restoring neuronal Mex3c expression, significantly increased white adipose tissue deposition, but had no effects on body length. Our data suggest that one way in which Mex3c regulates adiposity is through controlling physical activity, and that neuronal Mex3c expression could play an important role in this process.

摘要

Mex3C 是一种 RNA 结合蛋白,其生理功能未知。我们最近报道了小鼠的 Mex3c 突变会导致生长迟缓和脂肪减少,但脂肪减少的机制尚不清楚。在此,我们发现纯合子 Mex3c 基因捕获小鼠的体力活动增加。Mex3c 突变一致完全保护免受饮食诱导的肥胖、高血糖、胰岛素抵抗、高血脂和肝脂肪变性。在瘦素缺乏的 ob/ob 小鼠中,Mex3c 突变也增加了体力活动并改善了葡萄糖和脂质谱。在 Mex3c 基因捕获小鼠的神经元中表达 cre(一种试图部分恢复神经元 Mex3c 表达的方法),显著增加了白色脂肪组织的沉积,但对体长没有影响。我们的数据表明,Mex3c 调节脂肪量的一种方式是通过控制体力活动,而神经元 Mex3c 的表达可能在这个过程中发挥重要作用。

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