Modulation of glucose transport in skeletal muscle by reactive oxygen species

被引:49
作者
Katz, Abram [1 ]
机构
[1] Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden
关键词
exercise; adenosine 5 '-monophosphate-activated protein kinase; ACTIVATED PROTEIN-KINASE; HYDROGEN-PEROXIDE; INSULIN ACTION; TYROSINE PHOSPHORYLATION; TRANSVERSE TUBULES; UPSTREAM KINASE; IN-VIVO; EXERCISE; HYPOXIA; STIMULATION;
D O I
10.1152/japplphysiol.01066.2006
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Glucose transport is an essential physiological process that is characteristic of all eukaryotic cells, including skeletal muscle. In skeletal muscle, glucose transport is mediated by the GLUT-4 protein under conditions of increased carbohydrate utilization. The three major physiological stimuli of glucose transport in muscle are insulin, exercise/contraction, and hypoxia. Here, the role of reactive oxygen species (ROS) in modulating glucose transport in skeletal muscle is reviewed. Convincing evidence for ROS involvement in insulin- and hypoxia-mediated transport in muscle is lacking. Recent experiments, based on pharmacological and genetic approaches, support a role for ROS in contraction-mediated glucose transport. During contraction, endogenously produced ROS appear to mediate their effects on glucose transport via AMP-activated protein kinase.
引用
收藏
页码:1671 / 1676
页数:6
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