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首页> 外文期刊>Alcohol >Acute alcohol prevents the refeeding-induced decrease in autophagy but does not alter the increased protein synthetic response in heart
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Acute alcohol prevents the refeeding-induced decrease in autophagy but does not alter the increased protein synthetic response in heart

机译：急性醇防止再生诱导的自噬降低，但不会改变心脏中增加的蛋白质合成响应

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Ethanol produces a state of anabolic resistance in skeletal muscle; however, whether the heart displays a similar defect is unknown. Hence, the purpose of this study was to determine the impact of acute ethanol administration on the major signal transduction pathways in the heart that are responsible for regulating the protein synthetic and degradative response to refeeding. Adult male C57Bl/6 mice were fasted for 12 h. Mice were then either refed normal rodent chow for 30 min or a separate group of mice remained food deprived prior to administration of 3-g/kg ethanol. Cardiac tissue and blood were collected 1 h thereafter and analyzed. Acute ethanol prevented the nutrient-induced stimulation of S6K1 phosphorylation in heart, but did not alter the phosphorylation of S6, eIF4B, and eEF2, known downstream substrates for this kinase. The refeeding-induced redistribution of eIF4E into the active eIF4F complex was also not changed by acute ethanol. Consistent with the above-mentioned changes in signaling proteins, ethanol did not impair the refeeding-induced increase in cardiac protein synthesis. Proteasome activity was not altered by alcohol and/or refeeding. In contrast, ethanol antagonized the refeeding-induced increase in ULK1 phosphorylation and p62 as well as the reduction in LOB-II and Atg5/12 complex proteins. These data indicate that acute ethanol prevents the normally observed inhibition of autophagy seen after refeeding, while the mTOR-dependent increase in protein synthesis remains largely unaltered by alcohol. (C) 2018 Elsevier Inc. All rights reserved.
机译：乙醇在骨骼肌中产生了代谢性的状态;但是，心脏是否显示出类似的缺陷是未知的。因此，本研究的目的是确定急性乙醇给药对负责调节蛋白质合成和降解反应的心脏主要信号转导途径的影响。成年雄性C57BL / 6小鼠禁食12小时。然后在给予3g / kg乙醇之前，小鼠持续30分钟或单独的小鼠一组小鼠贫困的食物。此后收集心脏组织和血液并分析并分析。急性乙醇防止营养诱导的心脏S6K1磷酸化刺激，但没有改变S6，EIF4B和EEF2的磷酸化，该激酶的已知下游底物。 EIF4E进入活性EIF4F复合物的再诱导的再分布也没有通过急性乙醇改变。与上述信号蛋白的变化一致，乙醇并未损害了心脏蛋白合成的再生诱导的增加。蛋白酶体活性未被醇和/或再生改变。相反，乙醇拮抗了ulk1磷酸化和p62的再培养诱导的升高以及LOB-II和ATG5 / 12复合蛋白的减少。这些数据表明急性乙醇可防止在改进后看到的正常观察到的自噬抑制，而蛋白质合成的MTOR依赖性增加仍然受到醇的大大灭绝。 （c）2018年Elsevier Inc.保留所有权利。

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