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首页> 外文期刊>American Journal of Physiology >Protection of ischemic hearts by high glucose is mediated, in part, by GLUT-4.
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Protection of ischemic hearts by high glucose is mediated, in part, by GLUT-4.

机译：高血糖对缺血性心脏的保护部分是由GLUT-4介导的。

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摘要

Metabolic interventions that promote glucose use during ischemia have been shown to protect ischemic myocardium and improve functional recovery on reperfusion. We evaluated whether the cardioprotection afforded by high glucose during low-flow ischemia is associated with changes in the sarcolemmal content of glucose transporters, specifically GLUT-4. Isolated rat hearts were paced at 300 beats/min and perfused under normal glucose (5 mM) or high glucose (10 mM) conditions in buffer containing 0.4 mM albumin, 0.4 mM palmitate, and 70 mU/l insulin and subjected to 50 min of low-flow ischemia and 60 min of reperfusion. To determine the importance of insulin-sensitive glucose transporters in mediating cardioprotection, a separate group of hearts were perfused in the presence of cytochalasin B (10 microM), a preferential inhibitor of insulin-sensitive glucose transporters. Ischemic contracture during low-flow ischemia and creatine kinase release on reperfusion was decreased, and the percent recovery of left ventricular function with reperfusion was enhanced in hearts perfused with high glucose (P < 0.03). Hearts perfused with high glucose exhibited increased GLUT-4 protein expression in the sarcolemmal membrane compared with control hearts under baseline conditions, and these changes were additive with low-flow ischemia. In addition, high glucose did not affect the baseline distribution of sarcolemmal GLUT-1 and blunted any changes with low-flow ischemia. These salutary effects were abolished when glucose transporters are blocked with cytochalasin B. These data demonstrate that protection of ischemic myocardium by high glucose is associated with increased sarcolemmal content of the insulin-sensitive GLUT-4 and suggest a target for the protection of jeopardized myocardium.
机译：已显示在缺血期间促进葡萄糖使用的代谢干预措施可以保护缺血心肌，并改善再灌注时的功能恢复。我们评估了低流量缺血期间高糖提供的心脏保护作用是否与葡萄糖转运蛋白（尤其是GLUT-4）的肌膜含量变化相关。分离的大鼠心脏以300次/分钟的速度进行搏动，并在含有0.4 mM白蛋白，0.4 mM棕榈酸酯和70 mU / l胰岛素的缓冲液中，在正常葡萄糖（5 mM）或高葡萄糖（10 mM）条件下灌注，并进行50分钟的低流量缺血和60分钟的再灌注。为了确定胰岛素敏感性葡萄糖转运蛋白在介导心脏保护中的重要性，在细胞松弛素B（10 microM）（一种胰岛素敏感性葡萄糖转运蛋白的优先抑制剂）的存在下灌注了另一组心脏。低血流缺血期间的缺血性挛缩和再灌注时肌酸激酶的释放减少，并且在高葡萄糖灌注的心脏中，经再灌注可提高左心室功能的恢复百分比（P <0.03）。与基线状态下的对照心脏相比，灌注高葡萄糖的心脏在肌膜中显示出GLUT-4蛋白表达的增加，并且这些变化与低流量缺血有关。此外，高血糖不会影响肌膜GLUT-1的基线分布，并且不会因低流量缺血而改变任何变化。当葡萄糖转运蛋白被细胞松弛素B阻断时，这些有益的作用就被消除了。这些数据表明，高糖对缺血心肌的保护与胰岛素敏感性GLUT-4的肌膜含量增加有关，并提出了保护受损的心肌的靶标。

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