Obesity-induced insulin resistance and type 2 diabetes mellitus can ultimately result in various complications, including diabetic cardiomyopathy. In this case, cardiac dysfunction is characterized by metabolic disturbances such as impaired glucose oxidation and an increased reliance on fatty acid (FA) oxidation. Mitochondrial dysfunction has often been associated with the altered metabolic function in the diabetic heart, and may result from FA-induced lipotoxicity and uncoupling of oxidative phosphorylation. In this review, we address the metabolic changes in the diabetic heart, focusing on the loss of metabolic flexibility and cardiac mitochondrial function. We consider the alterations observed in mitochondrial substrate utilization, bioenergetics and dynamics, and highlight new areas of research which may improve our understanding of the cause and effect of cardiac mitochondrial dysfunction in diabetes. Finally, we explore how lifestyle (nutrition and exercise) and pharmacological interventions can prevent and treat metabolic and mitochondrial dysfunction in diabetes.

中文翻译：

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胰岛素抵抗性心脏的线粒体代谢发生改变。

肥胖引起的胰岛素抵抗和2型糖尿病最终可能导致各种并发症，包括糖尿病性心肌病。在这种情况下，心脏功能障碍的特征是代谢紊乱，例如葡萄糖氧化受损和对脂肪酸（FA）氧化的依赖性增加。线粒体功能障碍通常与糖尿病心脏的代谢功能改变有关，可能是由FA诱导的脂毒性和氧化磷酸化的解偶联引起的。在这篇综述中，我们着眼于糖尿病心脏的代谢变化，重点是代谢灵活性和心脏线粒体功能的丧失。我们考虑在线粒体底物利用率，生物能学和动力学方面观察到的变化，并重点介绍一些新的研究领域，这些领域可能会增进我们对糖尿病性心脏线粒体功能障碍的因果关系的了解。最后，我们探索生活方式（营养和运动）和药物干预措施如何预防和治疗糖尿病的代谢和线粒体功能障碍。