Activation of stat3 signaling in AgRP neurons promotes locomotor activity
Activation of stat3 signaling in AgRP neurons promotes locomotor activity
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激活 AgRP 神经元中的 stat3 信号可促进运动活动
DOI：
10.1016/j.cmet.2008.01.007
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发表时间：
2008-03-01
期刊：
影响因子：
29
通讯作者：
Bruening, Jens C.
中科院分区：
文献类型：
--
作者：
Mesaros, Andrea;Koralov, Sergei B.;Bruening, Jens C.
瘦素是一种脂肪细胞来源的激素，作用于位于下丘脑弓状核(ARC)的下丘脑神经元，调节能量平衡。ARC中瘦素调节的神经元亚型之一是刺鼠相关肽(AgRP)表达的神经元，它们参与食物摄取的调节，并直接被瘦素抑制。瘦素激活信号转导和转录激活子3(STAT3)，但STAT3对AgRP神经元的调节作用尚不清楚。在这里，我们展示了选择性地在AgRP神经元中表达STAT3的结构活性版本的小鼠是瘦小的，并对饮食诱导的肥胖表现出相对的抵抗力。令人惊讶的是，这种表型是在AgRP表达未改变的情况下运动活性增加所致。这些数据表明，ARC内AgRP神经元中的STAT3依赖的信号不依赖于AgRP的调节来控制运动活动。
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.