首页  期刊介绍 征稿简则 编委会 期刊征订 广告服务 留言板 联系我们 English

中国应用生理学杂志 ›› 2020, Vol. 36 ›› Issue (1): 12-16.doi: 10.12047/j.cjap.5802.2020.003

• 研究论文 • 上一篇    下一篇

急、慢性运动对2型糖尿病大鼠脂肪PI3K/AKT/GLUT4通路的影响

衣雪洁1, 孙玉霞1, 姚婷婷1, 李晶1, 高畅1, 刘璐1, 曹师承2△, 常波1, 张翠萍1   

  1. 1. 沈阳体育学院运动人体科学学院, 辽宁 沈阳 110102;
    2. 中国医科大学公共基础学院运动医学教研室, 辽宁 沈阳 110001
  • 出版日期:2020-01-28 发布日期:2020-06-01
  • 基金资助:
    E-mail: caoshicheng6666@163.com

Effects of acute and chronic exercise on fat PI3K/AKT/GLUT4 signal pathway in type 2 diabetic rats

YI Xue-jie1, SUN Yu-xia1, YAO Ting-ting1, LI Jing1, GAO Chang1, LIU Lu1, CAO Shi-cheng2△, CHANG Bo1, ZHANG Cui-ping1   

  1. 1. School of Sports and Human Sciences, Shenyang Sport University, Shenyang 110102;
    2. Department of Sports Medicine, School of Public and Basic Sciences, China Medical University, Shenyang 110001, China
  • Online:2020-01-28 Published:2020-06-01

摘要: 目的:探讨急性和慢性运动对2型糖尿病(T2DM)大鼠脂肪组织明磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(AKT)/葡萄糖运载体4(GLUT4)信号通路的影响。方法:15月龄SD雄性大鼠52只随机分为正常对照组(n=13)和高脂组(n=39),分别喂养普通和高脂饲料。8周后,高脂组体重>正常对照组20%,注射小剂量STZ后,血糖>16.7 mmol/l,造模成功。将糖尿病模型组随机分为糖尿病对照组(DC,n=13),糖尿病慢性运动组(DCE,n=13),糖尿病急性运动组(DAE,n=13)。DCE组进行8周的游泳运动,DAE组进行一次性游泳运动。测定血脂,血糖和血清胰岛素,Western blot法测定脂肪PI3K、AKT和GLUT4蛋白含量。结果:糖尿病组体重、血脂、血糖、胰岛素显著高于正常对照组(P均<0.01);高密度脂蛋白胆固醇(HDL-C)水平降低(P<0.05),脂肪组织中PI3K、AKT和GLUT4蛋白表达下降(P均<0.01)。糖尿病慢性运动组体重、血脂、血糖、胰岛素均出现显著性下降(P均<0.01);HDL-C升高(P<0.05),脂肪PI3K、AKT和GLUT4蛋白表达上升(P<0.01)。糖尿病急性运动组血脂、血糖、胰岛素下降(P均<0.05);HDL-C升高(P<0.05),脂肪PI3K、AKT和GLUT4含量显著上升(P均<0.05)。结论:①高脂饮食结合小剂量STZ诱导的T2DM大鼠脂肪组织PI3K/AKT通路受损,降低了胰岛素的敏感性。②急性、慢性有氧运动,均可以通过PI3K/AKT通路,改善糖脂代谢紊乱,慢性运动略优于急性运动。

关键词: 2型糖尿病, 脂肪, 运动, 磷脂酰肌醇3激酶/蛋白激酶B/葡萄糖转运载体4信号通路, 大鼠

Abstract: Objective: To study the effects of acute and chronic exercise on phosphatidylinositol 3-hydroxy kinase(PI3K)/protein kinase B(AKT)/glucose transporter 4(GLUT4)signaling pathway in adipose tissue of rats with type 2 diabetes mellitus (T2DM) induced by high-fat diet and low-dose streptozotocin (STZ). Methods: A total of 52 SD male rats aged 15 months were randomly divided into normal control group (13) and high-fat group (39), and fed normal and high fat diets. After 8 weeks, the body weight of the high-fat group was higher 20% than that of the normal control group. After a small dose of STZ, the blood glucose level was >16.7 mmol/l, and the model was successfully established. The diabetic model group was randomly divided into a diabetic control group (DC, n=13), a diabetic chronic exercise group (DCE, n=13), and a diabetic acute exercise group (DAE, n=13). The DCE group underwent an 8-week swimming exercise and the DAE group performed a one-time swimming exercise. Blood lipids, blood glucose and serum insulin levels were measured, and the contents of fat PI3K, AKT and GLUT4 proteins were determined by Western blot method.Results: The levels of body weight, blood lipids, blood glucose and insulin in the diabetic group were significantly higher than those in the normal control group (P<0.01); high density liptein cholesterol(HDL-C) levels were decreased (P<0.05), and the expressions of PI3K, AKT and GLUT4 protein in adipose tissue were decreased (P<0.01). After 8 weeks of swimming training, the levels of body weight, blood lipids, blood glucose and insulin all were decreased significantly (P<0.01); while the level of HDL-C was increased (P<0.05), and the expressions of PI3K, AKT and GLUT4 protein were increased (P<0.01). After acute exercise, the levels of blood lipids, blood glucose and insulin were decreased (P<0.05); the level of HDL-C was increased (P<0.05), and the expression levels of fat PI3K, AKT and GLUT4 were increased significantly (P<0.05).Conclusion: ①High fat diet combined with low-dose STZ induced damage to the PI3K/AKT pathway in adipose tissue of T2DM rats reduced insulin sensitivity. ②Acute and chronic aerobic exercise can improve the disorder of glucose and lipid metabolism through PI3K/AKT pathway, and the chronic exercise is better than acute exercise.

Key words: type 2 diabetes, fat, exercise, phosphatidylinositol 3 kinase/protein kinase B/glucose transporter 4, rat

版权所有 © 2015 《中国应用生理学杂志》编辑部
京ICP备16058274号-1
地址:天津市和平区大理道1号,邮编:300050  电话:022-84655184  E-mail:tjzgyish@163.com
本系统由北京玛格泰克科技发展有限公司设计开发 技术支持:support@magtech.com.cn