Application of Leptin in Enhancing Immunity and Maintaining Obesity

Gudisa Bereda
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Abstract

Leptin is predominantly generated in adipose tissue and circulates in serum both as a free and as a protein‐bound entity. Leptin, a 16 kDa nonglycosylated polypeptide product of the obese (ob) gene, is an adipocyte-derived hormone which has long been recognized as a key factor in regulating a wide range of biological responses involving energy homeostasis, neuroendocrine function, angiogenesis, bone formation and reproduction. Leptin is a key afferent signal linking adiposity level and nutritional status to neuroendocrine regulation of energy homeostasis chiefly through decrement in caloric uptake and enhancement in energy expenditure. Serum levels of leptin reflect the amount of energy stored in adipose tissue. Short-term energy imbalance as well as serum levels of several cytokines and hormones influence circulating leptin levels. Leptin acts by binding to specific receptors in the hypothalamus to change the expression of several neuropeptides that regulate neuroendocrine role and energy uptake and expenditure. Leptin plays a significant function in the pathogenesis of obesity and eating disorders and is thought to mediate the neuroendocrine response to food deprivation
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瘦素在增强免疫力和维持肥胖中的应用
瘦素主要在脂肪组织中产生,并以游离体和蛋白结合体的形式在血清中循环。瘦素是肥胖(ob)基因的一种16 kDa的非糖基化多肽产物,是一种脂肪细胞来源的激素,长期以来被认为是调节一系列生物反应的关键因素,包括能量稳态、神经内分泌功能、血管生成、骨形成和生殖。瘦素是将肥胖水平和营养状况与能量稳态的神经内分泌调节联系起来的关键传入信号,主要通过减少热量摄取和增加能量消耗。血清瘦素水平反映脂肪组织中储存的能量。短期能量失衡以及血清中几种细胞因子和激素水平影响循环瘦素水平。瘦素通过与下丘脑的特定受体结合来改变几种神经肽的表达,这些神经肽调节神经内分泌的作用和能量的摄取和消耗。瘦素在肥胖和饮食失调的发病机制中发挥重要作用,并被认为介导食物剥夺的神经内分泌反应
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