运动增加肥胖和2型糖尿病患者体内GLP-1水平的机制及意义

张奇龙 , 王晓慧*
上海体育学院运动科学学院,上海 200438

摘 要:

胰高血糖素样肽-1 (glucagon-like peptide-1, GLP-1)的减少在肥胖和2型糖尿病(type 2 diabetes mellitus, T2DM)中的重要作用为运动降低体重和血糖、改善胰岛素敏感性,以及防治肥胖及T2DM的机制研究提供了一个新视角。近年来的研究发现,运动可能通过谷氨酰胺(glutamine, Gln)、白介素-6 (interleukin-6, IL-6)、游离脂肪酸(free fatty acid, FFA)、交感-肾上腺髓质系统介导GLP-1的增加。增加的GLP-1可发挥改善胰岛β细胞功能,促进β细胞增殖、抑制β细胞凋亡、抑制食欲和胃排空以及降低chemerin等作用,从而提高胰岛素敏感性、减少能量摄入和改善血糖水平。这可能是运动防治肥胖、T2DM的机制之一,但仍需更多研究证实。该文就运动增加肥胖和2型糖尿病患者体内GLP-1水平的作用、机制及其生物学意义做一综述。

通讯作者:王晓慧 , Email:wangpan96@126.com

Mechanism and significance of exercise-induced increase of GLP-1 in obesity and type 2 diabetes
ZHANG Qi-Long , WANG Xiao-Hui*
School of Kinesiology, Shanghai University of Sport, Shanghai 200438, China

Abstract:

The important role of decreased glucagon-like peptide-1 (GLP-1) in obesity and type 2 diabetes mellitus (T2DM) provides a new perspective for the mechanisms of exercise-induced reductions of weight and plasma glucose, improvement of insulin sensitivity, as well as prevention and treatment of obesity and T2DM. Recent studies have found that exercise induced the increase of GLP-1 through the mediation of glutamine (Gln), interleukin-6 (IL-6), free fatty acids (FFA), and the sympathetic-adrenal medulla system. The increased GLP-1 resulted in the improved function of islet β cell, pro-proliferation and anti-apoptosis of β cell, suppressed appetite, inhibited gastric emptying and reduced chemerin, thus increasing insulin sensitivity, reducing energy intake and plasma glucose levels. This may be one of the mechanisms of exercise-mediated preventing and treating obesity and T2DM, but needs to be further confirmed. This article summarized the role of exercise-induced increase of GLP-1 in obesity and T2DM and its significance and mechanism.

Communication Author:WANG Xiao-Hui , Email:wangpan96@126.com

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