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首页> 外文期刊>Cell metabolism >Orexin is required for brown adipose tissue development, differentiation, and function.
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Orexin is required for brown adipose tissue development, differentiation, and function.

机译：食欲素是棕色脂肪组织发育，分化和功能所必需的。

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摘要

Orexin (OX) neuropeptides stimulate feeding and arousal. Deficiency of orexin is implicated in narcolepsy, a disease associated with obesity, paradoxically in the face of reduced food intake. Here, we show that obesity in orexin-null mice is associated with impaired brown adipose tissue (BAT) thermogenesis. Failure of thermogenesis in OX-null mice is due to inability of brown preadipocytes to differentiate. The differentiation defect in OX-null neonates is circumvented by OX injections to OX-null dams. In vitro, OX, triggers the full differentiation program in mesenchymal progenitor stem cells, embryonic fibroblasts and brown preadipocytes via p38 mitogen activated protein (MAP) kinase and bone morphogenetic protein receptor-1a (BMPR1A)-dependent Smad1/5 signaling. Our study suggests that obesity associated with OX depletion is linked to brown-fat hypoactivity, which leads to dampening of energy expenditure. Thus, orexin plays an integral role in adaptive thermogenesis and body weight regulation via effects on BAT differentiation and function.
机译：食欲素（OX）神经肽刺激进食和唤醒。食欲不振与食欲不振有关，这是与肥胖症有关的发作性睡病。在这里，我们表明，肥胖症的食欲素无效小鼠与棕色脂肪组织（BAT）生热受损有关。 OX空小鼠的生热失败是由于棕色前脂肪细胞无法分化所致。 OX无效母婴的OX注射可避免OX无效新生儿的分化缺陷。在体外，OX通过p38促分裂原活化蛋白（MAP）激酶和骨形态发生蛋白受体1a（BMPR1A）依赖性Smad1 / 5信号触发了间充质祖细胞，胚胎成纤维细胞和棕色前脂肪细胞的完全分化程序。我们的研究表明，与OX耗竭相关的肥胖与棕脂机能减退有关，这导致能量消耗的减少。因此，食欲肽通过影响BAT的分化和功能，在适应性生热和体重调节中起着不可或缺的作用。

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