van Dijk G
Department of Animal Physiology, Division Neuroendocrinology, School of Behavioural and Cognitive Neurosciences, University of Groningen, Haren, The Netherlands.
J Neuroendocrinol. 2001 Oct;13(10):913-21. doi: 10.1046/j.1365-2826.2001.00707.x.
Since its discovery, leptin (a 167-amino acid product of the OB gene) has quickly moved to the forefront as an important hormone for regulation of energy balance. It closes a feedback loop from adipose tissue to hypothalamic neuropeptide-containing neural circuitry involved in regulation of food intake and neuroendocrine/autonomic outflow. While increased central leptin signalling reduces adiposity via a reduction in food intake, it also has remarkable metabolic effects that promote leanness, independent of food intake. These include: (i) increased energy expenditure, (ii) in-place degradation of fat, and (iii) increased thermogenesis. Hypothalamic neurones that synthesize corticotropin releasing hormone and melanocortins (i.e. alpha-melanocyte-stimulating hormone and agouti-related protein) are likely effector pathways that mediate the anorexigenic and metabolic effects of leptin. Activation of sympathetic outflow (via neuropeptidergic effector pathways of central leptin) to a number of tissues that store fat might be an important mechanism through which these peripheral metabolic effects are elicited. It is proposed that these peripheral metabolic effects contribute to the satiating properties of leptin.
自发现以来，瘦素（OB基因的一种含167个氨基酸的产物）迅速成为调节能量平衡的重要激素，处于前沿地位。它形成了一个从脂肪组织到下丘脑含神经肽的神经回路的反馈环，该神经回路参与食物摄入调节以及神经内分泌/自主神经输出。虽然中枢瘦素信号增强通过减少食物摄入量来降低肥胖程度，但它还具有显著的代谢作用，可促进消瘦，且与食物摄入量无关。这些作用包括：（i）能量消耗增加，（ii）脂肪就地降解，以及（iii）产热增加。合成促肾上腺皮质激素释放激素和黑皮质素（即α-促黑素细胞激素和刺鼠相关蛋白）的下丘脑神经元可能是介导瘦素厌食和代谢作用的效应途径。通过交感神经输出（经由中枢瘦素的神经肽能效应途径）激活多个储存脂肪的组织，可能是引发这些外周代谢作用的重要机制。有人提出，这些外周代谢作用有助于瘦素的饱腹感特性。
