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Mex3c Mutation Reduces Adiposity and Increases Energy Expenditure

机译：Mex3c突变可减少肥胖症并增加能量消耗

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The function of MEX3C, the mammalian homolog of Caenorhabditis elegans RNA-binding protein muscle excess 3 (MEX-3), was unknown until our recent report that MEX3C is necessary for normal postnatal growth and enhances the expression of local bone Igf1 expression. Here we report the pivotal role of Mex3c in energy balance regulation. Mex3c mutation caused leanness in both heterozygous and homozygous transgenic mice, as well as a more beneficial blood glucose and lipid profile in homozygous transgenic mice, in both sexes. Although transgenic mice showed normal food intake and fecal lipid excretion, they had increased energy expenditure independent of physical activity. Mutant mice had normal body temperature, Ucp1 expression in brown adipose tissue, and muscle and liver fatty acid oxidation. Mex3c is expressed in neurons and is detectable in the arcuate nucleus, the ventromedial nucleus, and the dorsomedial nucleus of the hypothalamus. Mex3c was not detected in NPY or POMC neurons but was detected in leptin-responsive neurons in the ventromedial nucleus. Mex3c and Leptin double mutant mice were growth retarded and obese and had blood profiles similar to those of ob/ob mice but showed none of the steatosis observed in ob/ob mice. Our data show that Mex3c is involved in energy balance regulation.
机译：MEX3C的功能，即秀丽隐杆线虫RNA结合蛋白肌肉过量3（MEX-3）的哺乳动物同源物，直到我们最近的报道MEX3C对于正常的出生后生长并增强局部骨 Igf1 < / em>表达式。在这里，我们报告 Mex3c 在能量平衡调节中的关键作用。 Mex3c 突变在杂合和纯合转基因小鼠中均导致瘦弱，并且在两性中均在纯合转基因小鼠中引起更有益的血糖和脂质分布。尽管转基因小鼠显示出正常的食物摄入和粪便脂质排泄，但它们的能量消耗增加而与体力活动无关。突变小鼠的体温正常，棕色脂肪组织中的 Ucp1 表达，肌肉和肝脏的脂肪酸氧化。 Mex3c 在神经元中表达，可在下丘脑的弓形核，腹膜内侧核和背侧核中检测到。在NPY或POMC神经元中未检测到 Mex3c ，而在腹内侧核的瘦素反应性神经元中检测到了。 Mex3c 和 Leptin 双重突变小鼠生长迟缓和肥胖，血液特征与 ob / ob 小鼠相似，但均未显示脂肪变性在 ob / ob 小鼠中观察到。我们的数据表明 Mex3c 参与能量平衡调节。

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