Leptin and its mechanism of action

A. Panic, Sanja Soskić, E. Isenovic
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Abstract

Leptin is a hormone produced by the adipose tissue, which has effects on the central nervous system. Leptin is bound to its Ob receptor on hypo-thalamic neurons to inhibit feeding behavior and to increase sympathetically-mediated thermogenesis. In addition to anorexia and thermogenesis, leptin also has direct peripheral and central nervous system-mediated effects on the endocrine, vascular, hematopoietc, immune and musculoskeletal systems. Leptin accomplishes its effects using distributed network of leptin receptors and differential molecular signaling pathways. Leptinemia is increased in obesity because of increased adipocyte mass, but obese subjects exhibit resistance to the anorexic and metabolic effects of leptin. However, multiple studies have shown that leptin can increase sympathetic nerve activity to non-thermogenic tissues in rodents causing obesity-related hypertension. One potential explanation of this paradox is selective leptin resistance. Compared with large and persuasive number of studies on the sympathetic and blood pressure effects of leptin in experimental animals, relatively little attention was given to these effects of leptin in humans. This review article presents recent findings related to leptin and its mechanism of action, and also the role of leptin in patophysiological conditions.
瘦素及其作用机制
瘦素是一种由脂肪组织产生的激素,对中枢神经系统有影响。瘦素与其下丘脑神经元上的Ob受体结合,抑制摄食行为并增加交感神经介导的产热作用。除了厌食和产热,瘦素还对内分泌、血管、造血、免疫和肌肉骨骼系统有直接的外周和中枢神经系统介导的作用。瘦素通过分布的瘦素受体网络和不同的分子信号通路来实现其作用。由于脂肪细胞质量增加,肥胖患者瘦素血症增加,但肥胖受试者对瘦素的厌食和代谢作用表现出抵抗。然而,多项研究表明,瘦素可以增加啮齿动物非产热组织的交感神经活动,导致肥胖相关的高血压。这种矛盾的一个可能解释是选择性瘦素抵抗。与大量有说服力的关于瘦素在实验动物中对交感神经和血压影响的研究相比,对瘦素在人类中的这些影响的关注相对较少。本文综述了近年来有关瘦素及其作用机制的研究进展,以及瘦素在病理生理条件下的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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