运动改善肥胖症瘦素抵抗及其机制研究进展

大部分肥胖患者体内出现瘦素抵抗,表现为血清瘦素水平异常升高,但机体对瘦素不敏感或无反应,使瘦素抑制食欲、增加能量消耗和降低血糖等功能不能有效发挥.减轻瘦素抵抗被认为是治疗肥胖及肥胖相关疾病的有效途径.运动减轻肥胖、改善糖脂代谢和增强胰岛素敏感性的作用与运动降低瘦素水平、改善瘦素抵抗密切相关.本文在概述瘦素实现生理功能的机制、肥胖症的中枢及外周瘦素抵抗的基础上,主要综述近年来运动减轻肥胖症瘦素抵抗机制的研究进展,包括减轻高瘦素血症、改善中枢和外周瘦素抵抗,以期为运动防治肥胖机制的研究提供新视角.

Progress in Exercise-induced Improvements of Leptin Resistance in Obese Subjects and Its Mechanisms

Most of obese subjects show leptin resistance, characterized by abnormal increase of serum leptin but diminished effects of leptin on inhibiting appetite, enhancing energy expenditure and decreasing blood glucose. Reducing leptin resistance is considered as an effective strategy to treat obesity and obesity related diseases. Exercise decreases obesity, improves glycolipid metabolism and increases insulin sensitivity, which are closely related to exercise-induced decrease of serum leptin and alleviation of leptin resistance. This review mainly summarized the mechanisms of exercise-induced improvements of leptin resistance in obesity, including lowering hyperleptinaemia and decreasing central and peripheral leptin resistance. Alleviation of hyperleptinaemia in obesity by exercise attributes to decreased fat mass and improved inflammation. For the decrease of central leptin resistance in obesity, exercise modulates neurons activities (stimulating SF-1, POMC neurons and inhibiting AgRP neurons) and other molecules related to energy metabolic homeostasis and food intake (elevating hypothalamic IL-6), and regulates expressions of proteins involved in leptin signaling of hypothalamus (stimulating STAT3, and inhibiting PTP1B and SOCS3); while exercise-induced decrease of peripheral leptin resistance comes from improvements of body composition (decreased fat mass, increased brown adipose tissue and reduced inflammation) and regulation of protein expressions involved in leptin signaling in muscle and liver (inhibiting SOCS3 and PTP1B). This review could provide a new insight into the mechanism of exercise-mediated prevention and treatment of obesity.