Frontiers: Skeletal muscle sodium pump regulation: a translocation paradigm

被引:33
作者
Benziane, Boubacar [1 ]
Chibalin, Alexander V. [1 ]
机构
[1] Karolinska Inst, Dept Mol Med & Surg, Sect Integrat Physiol, S-17177 Stockholm, Sweden
来源
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM | 2008年 / 295卷 / 03期
基金
瑞典研究理事会;
关键词
Na+-K+-ATPase; translocation; insulin; contraction; membrane traffic; ouabain;
D O I
10.1152/ajpendo.90261.2008
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The skeletal muscle sodium pump plays a major role in the removal of K+ ions from the circulation postprandial, or after a physical activity bout, thereby preventing the development of hyperkalemia and fatigue. Insulin and muscle contractions stimulate Na+-K+-ATPase activity in skeletal muscle, at least partially via translocation of sodium pump units to the plasma membrane from intracellular stores. The molecular mechanism of this phenomenon is poorly understood. Due to the contradictory reports in the literature, the very existence of the translocation of Na+-K+-ATPase to the skeletal muscle cell surface is questionable. This review summarizes more than 30 years work on the skeletal muscle sodium pump translocation paradigm. Furthermore, the methodological caveats of major approaches to study the sodium pump translocation in skeletal muscle are discussed. An understanding of the molecular regulation of Na+-K+-ATPase in skeletal muscle will have important clinical implications for the understanding of the development of complications associated with the metabolic syndrome, such as cardiovascular diseases or increased muscle fatigue in diabetic patients.
引用
收藏
页码:E553 / E558
页数:6
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