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首页> 外文期刊>American Journal of Physiology >Regulation of cardiac malonyl-CoA content and fatty acid oxidation during increased cardiac power.
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Regulation of cardiac malonyl-CoA content and fatty acid oxidation during increased cardiac power.

机译：心脏功率增加期间心脏丙二酰辅酶A含量和脂肪酸氧化的调节。

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摘要

Myocardial fatty acid oxidation is regulated by carnitine palmitoyltransferase I (CPT I), which is inhibited by malonyl-CoA. Increased cardiac power causes a fall in malonyl-CoA content and accelerated fatty acid oxidation; however, the mechanism for the decrease in malonyl-CoA is unclear. Malonyl-CoA is formed by acetyl-CoA carboxylase (ACC) and degraded by malonyl-CoA decarboxylase (MCD); thus a fall in malonyl-CoA could be due to activation of MCD, inhibition of ACC, or both. This study assessed the effects of increased cardiac power on malonyl-CoA content and ACC and MCD activities. Anesthetized pigs were studied under control conditions and during increased cardiac power in response to dobutamine infusion and aortic constriction alone, under hyperglycemic conditions, or with the CPT I inhibitor oxfenicine. An increase in cardiac power was accompanied by increased myocardial O(2) consumption, decreased malonyl-CoA concentration, and increased fatty acid oxidation. There were no differences among groups in activity of ACC or AMP-activated protein kinase (AMPK), which physiologically inhibits ACC. There also were no differences in V(max) or K(m) of MCD. Previous studies have demonstrated that AMPK can be inhibited by protein kinase B (PKB); however, PKB was activated by dobutamine and the elevated insulin that accompanied hyperglycemia, but there was no effect on AMPK activity. In conclusion, the fall in malonyl-CoA and increase in fatty acid oxidation that occur with increased cardiac work were not due to inhibition of ACC or activation of MCD, suggesting alternative regulatory mechanisms for the work-induced decrease in malonyl-CoA concentration.
机译：心肌脂肪酸的氧化受肉碱棕榈酰转移酶I（CPT I）的调节，而丙二酰辅酶A可以抑制该酶。心脏功率增加会导致丙二酰辅酶A含量下降并加速脂肪酸氧化;但是，丙二酰辅酶A降低的机理尚不清楚。丙二酰辅酶A由乙酰辅酶A羧化酶（ACC）形成，并被丙二酰辅酶A脱羧酶（MCD）降解。因此，丙二酰辅酶A的下降可能是由于MCD的激活，ACC的抑制或两者兼而有之。这项研究评估了心脏功率增加对丙二酰辅酶A含量以及ACC和MCD活性的影响。在高血糖条件下或在使用CPT I抑制剂奥芬尼辛的情况下，仅在多巴酚丁胺输注和主动脉收缩的情况下，在对照条件下和在心脏功率增加期间对麻醉猪进行了研究。心力的增加伴随着心肌O（2）消耗的增加，丙二酰辅酶A浓度的降低和脂肪酸氧化的增加。两组之间在生理上抑制ACC的ACC或AMP活化蛋白激酶（AMPK）的活性无差异。 MCD的V（max）或K（m）也没有差异。先前的研究表明，AMPK可以被蛋白激酶B（PKB）抑制。但是，多巴酚丁胺和伴随高血糖的胰岛素升高激活了PKB，但对AMPK活性没有影响。总之，随着心脏功的增加而发生的丙二酰辅酶A的下降和脂肪酸氧化的增加并不是由于抑制ACC或MCD的激活所致，提示了由工作引起的丙二酰辅酶A浓度降低的替代调控机制。

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