Heart failure is a disorder of aging. Its prevalence is amplified in the presence of diabetes. The heart metabolizes many available substances to support its constant need for adenosine triphosphate (ATP) to fuel myocardial contraction. Quantitatively, fatty acid oxidation generates more than 60% of myocardial ATP with the remainder coming from lactate and glucose. In heart failure and diabetes, the relative contribution of these metabolites is altered. Recent studies have revealed that changes in patterns of glucose utilization in the failing heart and in diabetes activate non-ATP generating metabolic pathways that directly activate pathways that promote myocardial remodeling in the failing heart. In this webinar, E. Dale Abel, MD, PhD, from the University of Iowa, will present recent studies revealing novel mechanisms by which perturbed metabolism of glucose and pyruvate contribute to the pathophysiology of heart failure.