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.

中文翻译：

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瘦素作用和瘦素抵抗的机制。

源自脂肪组织的激素瘦素通过其在大脑中的受体（LRb）起作用，以调节能量平衡和神经内分泌功能。瘦素作用的整体需要经由STAT3和许多其他途径的LRb信号传导。瘦素水平升高未能抑制常见肥胖症的进食和介导体重减轻，这定义了所谓的瘦素抵抗状态。多种机制，包括瘦素刺激的LRb上的Tyr（985）磷酸化和细胞因子信号传导抑制剂3，都减弱了瘦素信号传导并促进了肥胖症中细胞对瘦素的抵抗力。下丘脑弓形核的几个独特特征可能会导致该区域细胞瘦素抵抗的严重性。