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November 16, 2021
11 a.m. EST

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.

Speaker

Dale Abel 200E. Dale Abel, MD, PhD, is the chair and department executive officer of the Department of Internal Medicine and director of the Fraternal Order of Eagles Diabetes Research Centerat the University of Iowa. He is a professor of medicinebiochemistry and biomedical engineering. Abel holds the John B. Stokes III Chair in Diabetes Research and the François M. Abboud Chair in Internal Medicine. His pioneering work on glucose transport and mitochondrial metabolism in the heart guides his current research interests, including the molecular mechanisms responsible for cardiovascular complications of diabetes. Abel’s laboratory has provided important insights into the contribution of mitochondrial dysfunction and aberrant insulin signaling, to heart failure risk in diabetes. Recent work has focused on mitochondrial mechanisms that mediate inter-organ crosstalk that may influence the pathophysiology of insulin resistance and mitochondrial pathways linking metabolism with increased risk for atherothrombosis. 

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