Cardiac-Specific GLUT1 Overexpression Preserves Contractile Reserve in Diabetic Mouse Hearts: a Multi-Phase DENSE MRI Study under Dobutamine-Induced Cardiac Stress

Introduction Diabetes mellitus is associated with increased cardiac morbidity and mortality. Cardiomyopathy occurs commonly in diabetics independent of known risk factors such as coronary artery disease or hypertension. Although the underlying mechanism is multifactorial, evidences are emerging towards metabolic disturbance that may play a causal role in modulating myocardial contractile performance and the pathogenesis of diabetic cardiomyopathy (1,2). In our previous study, we found normalized basal cardiac function in diabetic mice with cardiac-specific overexpression of a basal cardiac glucose transporter, GLUT1. In the current study, we aimed to test the hypothesis that contractile reserve in Type I diabetic mouse hearts is preserved by metabolic modulation through GLUT1 overexpression. Such preservation will lead to normalized β-adrenergic response. To test this hypothesis, we investigated cardiac functions in diabetic mouse hearts using multi-phase MR Displacement Encoding with Stimulated Echoes (DENSE) under dobutamine-induced cardiac stress.