Exercise, glucose transport, and insulin sensitivity

被引:741
作者
Goodyear, LJ [1 ]
Kahn, BB
机构
[1] Brigham & Womens Hosp, Joslin Diabet Ctr, Div Res, Boston, MA 02215 USA
[2] Harvard Univ, Sch Med, Dept Med, Boston, MA 02215 USA
[3] Beth Israel Deaconess Med Ctr, Div Endocrinol & Metab, Diabet Unit, Boston, MA 02215 USA
来源
ANNUAL REVIEW OF MEDICINE | 1998年 / 49卷
关键词
skeletal muscle; GLUT4; diabetes; insulin resistance; physical training;
D O I
10.1146/annurev.med.49.1.235
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Physical exercise can be an important adjunct in the treatment of both non-insulin-dependent diabetes mellitus and insulin-dependent diabetes mellitus. Over the past several years, considerable progress has been made in understanding the molecular basis for these clinically important effects of physical exercise. Similarly to insulin, a single bout of exercise increases the rate of glucose uptake into the contracting skeletal muscles, a process that is regulated by the translocation of GLUT4 glucose transporters to the plasma membrane and transverse tubules. Exercise and insulin utilize different signaling pathways, both of which lead to the activation of glucose transport, which perhaps explains why humans with insulin resistance can increase muscle glucose transport in response to an acute bout of exercise. Exercise training in humans results in numerous beneficial adaptations in skeletal muscles, including an increase in GLUT4 expression. The increase in muscle GLUT4 in trained individuals contributes to an increase in the responsiveness of muscle glucose uptake to insulin, although not all studies show that exercise training in patients with diabetes improves overall glucose control. However, there is now extensive epidemiological evidence demonstrating that long-term regular physical exercise can significantly reduce the risk of developing non-insulin-dependent diabetes mellitus.
引用
收藏
页码:235 / 261
页数:27
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