Neuromedin U has a novel anorexigenic effect independent of the leptin signaling pathway
Neuromedin U has a novel anorexigenic effect independent of the leptin signaling pathway
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DOI：
10.1038/nm1106
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发表时间：
2004-10-01
期刊：
影响因子：
82.9
通讯作者：
Kojima, M
中科院分区：
文献类型：
--
作者：
Hanada, R;Teranishi, H;Kojima, M
神经介肽U（NMU）是一种下丘脑神经肽，调节体重和组成。在这里，我们表明缺乏编码NMU的基因的小鼠（Nmu（-/-）小鼠）会出现肥胖。Nmu（-/-）小鼠表现出体重增加和肥胖，摄食量增加，运动活动和能量消耗减少。肥胖Nmu（-/-）小鼠出现高瘦素血症、高胰岛素血症、迟发性高血糖和高脂血症。然而，值得注意的是，用外源性瘦素治疗在降低肥胖Nmu（-/-）小鼠的体重方面是有效的。此外，中枢瘦素给药并不影响大鼠下丘脑NMU基因的表达。这些结果表明，NMU在摄食行为和能量代谢的调节中起重要作用，而不依赖于瘦素信号通路。NMU的这些特征性功能可能为理解肥胖的病理生理基础提供新的见解。
Neuromedin U (NMU) is a hypothalamic neuropeptide that regulates body weight and composition. Here we show that mice lacking the gene encoding NMU (Nmu(-/-) mice) develop obesity. Nmu(-/-) mice showed increased body weight and adiposity, hyperphagia, and decreased locomotor activity and energy expenditure. Obese Nmu(-/-) mice developed hyperleptinemia, hyperinsulinemia, late-onset hyperglycemia and hyperlipidemia. Notably, however, treatment with exogenous leptin was effective in reducing body weight in obese Nmu(-/-) mice. In addition, central leptin administration did not affect NMU gene expression in the hypothalamus of rats. These results indicate that NMU plays an important role in the regulation of feeding behavior and energy metabolism independent of the leptin signaling pathway. These characteristic functions of NMU may provide new insight for understanding the pathophysiological basis of obesity.