Abstract 3722: Diet-induced Weight Loss Improves Myocardial Glycolysis and Glucose Oxidation Rates in Obese Humans
Obesity contributes to the development of cardiac dysfunction in animal studies by excessively increasing myocardial fatty acid metabolism, which is at the expense of glucose metabolism. This disproportionate dependence on fatty acid is particularly detrimental when conditions that require glucose use (e.g., ischemia) are superimposed. Whether weight loss can restore myocardial metabolic flexibility and increase myocardial glucose metabolism in obese humans is unknown. This study tested the hypothesis that weight loss would increase myocardial glucose metabolism.
Methods: We studied 13 obese (body mass index>30kg/m2) adults before and after a 20-week physician-supervised weight loss program. Subjects were injected with 1-11C-glucose and then underwent positron emission tomography (PET) imaging. The PET images and time-activity curves were analyzed in conjunction with well-validated mathematical modeling in order to quantify myocardial glucose utilization, glycolysis, glycogen synthesis, and glucose oxidation, and echocardiography was used to quantify cardiac structure and function pre- and post-weight loss.
Results: Diet-induced weight loss resulted in a significant 10% weight loss and concomitant improvements in rate-pressure product (mean change 783mmHg*bpm, p=0.03), and plasma insulin. Resting myocardial glycolysis, glucose oxidation, and glucose utilization/plasma insulin also significantly improved and myocardial glucose utilization trended toward improvement (Table⇓). Myocardial glycogen production, cardiac mass, and ejection fraction were unchanged.
Conclusions: Diet-induced weight loss in obese humans improves their myocardial glucose metabolism. This restoration of myocardial glucose metabolism should improve the heart’s metabolic flexibility and adaptability to varying conditions.