Flak Jonathan N, Myers Martin G
Division of Metabolism, Endocrinology and Diabetes (J.N.F., M.G.M.), Department of Internal Medicine, and Department of Molecular and Integrative Physiology (M.G.M.), University of Michigan, Ann Arbor, Michigan 48109.
Mol Endocrinol. 2016 Jan;30(1):3-12. doi: 10.1210/me.2015-1232. Epub 2015 Oct 20.
Leptin is an adipocytokine that circulates in proportion to body fat to signal the repletion of long-term energy stores. Leptin acts via its receptor, LepRb, on specialized neuronal populations in the brain (mainly in the hypothalamus and brainstem) to alter motivation and satiety, as well as to permit energy expenditure and appropriate glucose homeostasis. Decreased leptin, as with prolonged caloric restriction, promotes a powerful orexigenic signal, decreases energy use via a number of neuroendocrine and autonomic axes, and disrupts glucose homeostasis. Here, we review what is known about cellular leptin action and focus on the roles for specific populations of LepRb-expressing neurons for leptin action.
瘦素是一种脂肪细胞因子,其在血液中的循环水平与体脂成正比,用于传递长期能量储备充足的信号。瘦素通过其受体LepRb作用于大脑中的特定神经元群体(主要位于下丘脑和脑干),以改变动机和饱腹感,同时促进能量消耗并维持适当的葡萄糖稳态。与长期热量限制一样,瘦素水平降低会产生强烈的促食欲信号,通过多个神经内分泌和自主神经轴减少能量消耗,并破坏葡萄糖稳态。在此,我们综述了关于细胞瘦素作用的已知信息,并重点关注表达LepRb的特定神经元群体在瘦素作用中的作用。