Energy substrate metabolism in cardiac hypertrophy
Energy substrate metabolism in cardiac hypertrophy
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DOI：
10.1007/s11906-004-0036-2
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发表时间：
2004-12-01
影响因子：
5.6
通讯作者：
Allard, MF
中科院分区：
文献类型：
--
作者：
Allard, MF
心脏肥大是对长期病理性（例如高血压）或生理性（例如运动）血流动力学超负荷的反应，伴随着能量底物利用的变化。病理性和生理性心脏肥大之间的底物利用模式（或代谢表型）显着不同，脂肪酸和葡萄糖的氧化和糖酵解的变化方向相反。这些发现表明，对血流动力学负荷长期变化的代谢反应并非刻板印象，而是受到导致心脏肥大的刺激性质的影响。尽管底物利用的变化是适应性的，但在病理刺激的情况下，代谢的变化会干扰心脏对代谢应激的功能弹性，如缺血再灌注期间发生的情况。响应病理或生理刺激而肥大的心脏的独特代谢表型不仅是由于代谢酶和蛋白质表达的改变，而且是由于代谢酶和蛋白质的翻译后调节。
Cardiac hypertrophy is a response to long-term pathologic (eg, hypertension) or physiologic (eg, exercise) hemodynamic overload accompanied by changes in energy substrate utilization. The pattern of substrate utilization (or metabolic phenotype) differs dramatically between pathologic and physiologic cardiac hypertrophy with directionally opposite changes in oxidation of fatty acids and glucose and glycolysis. These findings indicate that the metabolic response to long-term alterations in hemodynamic workload is not stereotypical, but is influenced by the nature of the stimulus leading to cardiac hypertrophy. Although the changes in substrate utilization are adaptive, in the case of pathologic stimuli, the changes in metabolism interfere with functional resiliency of the heart to metabolic stress, as occurs during ischemia-reperfusion. The distinct metabolic phenotypes of hearts hypertrophied in response to pathologic or physiologic stimuli are due not only to alteration in expression of metabolic enzymes and proteins, but also to post-translational modulation of metabolic enzymes and proteins.