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慢性氮质血症和运动中胰岛素刺激的蛋白质代谢

Insulin-stimulated protein metabolism in chronic azotemia and exercise.

作者信息

Davis T A, Klahr S, Karl I E

出版信息

Am J Physiol. 1987 Jul;253(1 Pt 2):F164-9. doi: 10.1152/ajprenal.1987.253.1.F164.

DOI:10.1152/ajprenal.1987.253.1.F164
PMID:3300369
Abstract

To determine whether training reduces the acute catabolic stress of an exercise bout, control and azotemic rats, either exercise trained or untrained, were subjected to a bout of exercise or allowed to rest. Protein turnover was measured immediately following exercise in isolated muscles. Azotemia (no exercise) increased protein degradation; acute exercise (no azotemia) decreased protein synthesis. Protein catabolism was greatest in acutely exercised azotemic rats. Training reduced azotemia-induced and acute exercise-stimulated increase in protein degradation. To determine whether this improvement in protein metabolism by training was due to increased insulin sensitivity, the dose-response to insulin was determined. Resistance of protein synthesis or degradation to insulin was not observed in azotemic rats. Either acute exercise or training increased sensitivities of protein degradation and synthesis to insulin; training also increased responsiveness of protein degradation to insulin. Thus exercise training reduced the elevated muscle protein catabolism due to azotemia and/or acute exercise and enhanced the action of insulin on muscle.

摘要

为了确定训练是否能减轻运动 bout 的急性分解代谢应激,将对照大鼠和氮血症大鼠(无论是否经过运动训练)进行一次运动 bout 或使其休息。在运动后立即测量分离肌肉中的蛋白质周转率。氮血症(不运动)会增加蛋白质降解;急性运动(无氮血症)会降低蛋白质合成。急性运动的氮血症大鼠的蛋白质分解代谢最为显著。训练减少了氮血症诱导的以及急性运动刺激引起的蛋白质降解增加。为了确定训练对蛋白质代谢的这种改善是否归因于胰岛素敏感性增加,测定了对胰岛素的剂量反应。在氮血症大鼠中未观察到蛋白质合成或降解对胰岛素的抵抗。急性运动或训练均增加了蛋白质降解和合成对胰岛素的敏感性;训练还增加了蛋白质降解对胰岛素的反应性。因此,运动训练减少了因氮血症和/或急性运动导致的肌肉蛋白质分解代谢升高,并增强了胰岛素对肌肉的作用。

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Insulin-stimulated protein metabolism in chronic azotemia and exercise.慢性氮质血症和运动中胰岛素刺激的蛋白质代谢
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