Division of Diabetes, Department of Medicine, University of Texas Health, San Antonio, Texas, USA.
Department of Medicine, University of Mississippi School of Medicine, Jackson, Mississippi, USA.
J Am Coll Cardiol. 2021 Apr 27;77(16):2022-2039. doi: 10.1016/j.jacc.2021.02.057.
The mechanisms responsible for the positive and unexpected cardiovascular effects of sodium-glucose cotransporter-2 inhibitors and glucagon-like peptide-1 receptor agonists in patients with type 2 diabetes remain to be defined. It is likely that some of the beneficial cardiac effects of these antidiabetic drugs are mediated, in part, by altered myocardial metabolism. Common cardiometabolic disorders, including the metabolic (insulin resistance) syndrome and type 2 diabetes, are associated with altered substrate utilization and energy transduction by the myocardium, predisposing to the development of heart disease. Thus, the failing heart is characterized by a substrate shift toward glycolysis and ketone oxidation in an attempt to meet the high energetic demand of the constantly contracting heart. This review examines the metabolic pathways and clinical implications of myocardial substrate utilization in the normal heart and in cardiometabolic disorders, and discusses mechanisms by which antidiabetic drugs and metabolic interventions improve cardiac function in the failing heart.
钠-葡萄糖共转运蛋白 2 抑制剂和胰高血糖素样肽 1 受体激动剂在 2 型糖尿病患者中具有积极且出乎意料的心血管作用的机制仍有待确定。这些抗糖尿病药物的一些有益的心脏作用可能部分是通过改变心肌代谢来介导的。常见的心脏代谢紊乱，包括代谢（胰岛素抵抗）综合征和 2 型糖尿病，与心肌的底物利用和能量转导改变有关，易导致心脏病的发生。因此，衰竭的心脏表现为向糖酵解和酮体氧化的底物转移，以试图满足不断收缩的心脏的高能量需求。这篇综述探讨了正常心脏和心脏代谢紊乱中心肌底物利用的代谢途径和临床意义，并讨论了抗糖尿病药物和代谢干预改善衰竭心脏心功能的机制。
