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缺氧对骨骼肌葡萄糖转运的刺激作用。

Stimulation of glucose transport in skeletal muscle by hypoxia.

作者信息

Cartee G D, Douen A G, Ramlal T, Klip A, Holloszy J O

机构信息

Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110.

出版信息

J Appl Physiol (1985). 1991 Apr;70(4):1593-600. doi: 10.1152/jappl.1991.70.4.1593.

DOI:10.1152/jappl.1991.70.4.1593
PMID:2055841
Abstract

Hypoxia caused a progressive cytochalasin B-inhibitable increase in the rate of 3-O-methylglucose transport in rat epitrochlearis muscles to a level approximately six-fold above basal. Muscle ATP concentration was well maintained during hypoxia, and increased glucose transport activity was still present after 15 min of reoxygenation despite repletion of phosphocreatine. However, the increase in glucose transport activity completely reversed during a 180-min-long recovery in oxygenated medium. In perfused rat hindlimb muscles, hypoxia caused an increase in glucose transporters in the plasma membrane, suggesting that glucose transporter translocation plays a role in the stimulation of glucose transport by hypoxia. The maximal effects of hypoxia and insulin on glucose transport activity were additive, whereas the effects of exercise and hypoxia were not, providing evidence suggesting that hypoxia and exercise stimulate glucose transport by the same mechanism. Caffeine, at a concentration too low to cause muscle contraction or an increase in glucose transport by itself, markedly potentiated the effect of a submaximal hypoxic stimulus on sugar transport. Dantrolene significantly inhibited the hypoxia-induced increase in 3-O-methylglucose transport. These effects of caffeine and dantrolene suggest that Ca2+ plays a role in the stimulation of glucose transport by hypoxia.

摘要

缺氧导致大鼠肱三头肌中3 - O - 甲基葡萄糖转运速率出现细胞松弛素B可抑制的逐渐增加,达到比基础水平高约六倍的水平。在缺氧期间,肌肉ATP浓度保持良好,复氧15分钟后,尽管磷酸肌酸得到补充,但葡萄糖转运活性仍然存在。然而,在含氧培养基中180分钟的恢复过程中,葡萄糖转运活性的增加完全逆转。在灌注的大鼠后肢肌肉中,缺氧导致质膜中葡萄糖转运体增加,这表明葡萄糖转运体易位在缺氧刺激葡萄糖转运中起作用。缺氧和胰岛素对葡萄糖转运活性的最大作用是相加的,而运动和缺氧的作用则不是,这提供了证据表明缺氧和运动通过相同机制刺激葡萄糖转运。咖啡因浓度过低,本身不会引起肌肉收缩或增加葡萄糖转运,但能显著增强次最大缺氧刺激对糖转运的作用。丹曲林显著抑制缺氧诱导的3 - O - 甲基葡萄糖转运增加。咖啡因和丹曲林的这些作用表明Ca2 +在缺氧刺激葡萄糖转运中起作用。

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Stimulation of glucose transport in skeletal muscle by hypoxia.缺氧对骨骼肌葡萄糖转运的刺激作用。
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