Type 2 diabetes (T2D) substantially elevates the risk for heart failure, a major cause of death. In advanced T2D, energy metabolism in the heart is disrupted; glucose metabolism is decreased, fatty acid (FA) metabolism is enhanced to maintain ATP production, and cardiac function is impaired. This condition is termed diabetic cardiomyopathy (DCM). The exact cause of DCM is still unknown although altered metabolism is an important component. While type 2 diabetes is characterized by insulin resistance, the traditional antidiabetic agents that improve insulin stimulation or sensitivity only partially improve DCM-induced cardiac dysfunction. Recently, sodium-glucose transporter-2 (SGLT2) inhibitors have been identified as potential pharmacological agents to treat DCM. This review highlights the molecular mechanisms underlying cardiac energy metabolism in DCM, and the potential effects of SGLT2 inhibitors.
Copyright © 2020. Published by Elsevier Ltd.