瘦素
SOCS3
小鼠苗条素受体
内分泌学
下丘脑
脂肪组织
内科学
弓状核
脂肪因子
激素
受体
信号转导
生物
肥胖
医学
车站3
细胞生物学
作者
Martin G. Myers,Michael A. Cowley,Heike Münzberg
出处
期刊:Annual Review of Physiology
[Annual Reviews]
日期:2007-10-16
卷期号:70 (1): 537-556
被引量:992
标识
DOI:10.1146/annurev.physiol.70.113006.100707
摘要
The adipose tissue-derived hormone leptin acts via its receptor (LRb) in the brain to regulate energy balance and neuroendocrine function. LRb signaling via STAT3 and a number of other pathways is required for the totality of leptin action. The failure of elevated leptin levels to suppress feeding and mediate weight loss in common forms of obesity defines a state of so-called leptin resistance. A number of mechanisms, including the leptin-stimulated phosphorylation of Tyr(985) on LRb and the suppressor of cytokine signaling 3, attenuate leptin signaling and promote a cellular leptin resistance in obesity. Several unique features of the arcuate nucleus of the hypothalamus may contribute to the severity of cellular leptin resistance in this region. Other mechanisms that govern feeding behavior and food reward may also underlie the inception of obesity.
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