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首页> 外文期刊>Cell metabolism >Activation of Stat3 signaling in AgRP neurons promotes locomotor activity.
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Activation of Stat3 signaling in AgRP neurons promotes locomotor activity.

机译:AgRP神经元中Stat3信号的激活促进运动活性。

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摘要

Leptin, an adipocyte-derived hormone, acts on hypothalamic neurons located in the arcuate nucleus (ARC) of the hypothalamus to regulate energy homeostasis. One of the leptin-regulated neuronal subtypes in the ARC are agouti-related peptide (AgRP)-expressing neurons, which are involved in the regulation of food intake and are directly inhibited by leptin. Leptin activates the signal transducer and activator of transcription 3 (Stat3), but the role of Stat3 in the regulation of AgRP neurons is unclear. Here we show that mice expressing a constitutively active version of Stat3 selectively in AgRP neurons are lean and exhibit relative resistance to diet-induced obesity. Surprisingly, this phenotype arises from increased locomotor activity in the presence of unaltered AgRP expression. These data demonstrate that Stat3-dependent signaling in AgRP neurons in the ARC controls locomotor activity independently of AgRP regulation.
机译:瘦素是一种来自脂肪细胞的激素,作用于下丘脑弓状核(ARC)的下丘脑神经元,以调节能量稳态。 ARC中瘦素调节的神经元亚型之一是表达刺槐相关肽(AgRP)的神经元,其参与食物摄入的调节并被瘦素直接抑制。瘦蛋白激活信号转导和转录激活因子3(Stat3),但Stat3在调节AgRP神经元中的作用尚不清楚。在这里,我们显示在AgRP神经元中选择性表达Stat3组成型活性形式的小鼠是瘦的,并且对饮食诱导的肥胖表现出相对的抵抗力。出人意料的是,该表型是由于在未改变的AgRP表达的情况下运动能力增强而引起的。这些数据表明,ARC中AgRP神经元中依赖Stat3的信号传导独立于AgRP调节控制运动活性。

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