Abstract

Apolipoprotein E (ApoE) is necessary for normal lipid metabolism. A deficiency of this protein impedes plasma clearance of both triglycerides and cholesterol. These lipids are consequently broken down through alternate pathways, thus resulting in atypical cellular function. Cardiac mitochondria play a significant role in cellular respiration specifically, considering the extent of oxygen consumption that is required by the heart muscle. Their capacity to utilize oxygen and produce energy may be affected by the buildup of cholesterol and triglycerides, due to a deficiency in ApoE. This study will investigate the influence of ApoE deficiency on energy metabolism in young and older female mice. Whether or not any of these effects are exacerbated by further supplementation of lipids through diet will also be evaluated in male mice. Cardiac mitochondrial oxygen consumption, mitochondrial oxidative phosphorylation (OXPHOS) capacity and protein expression in cardiomyocytes will help in examining these influences. Our findings have the potential to provide important information regarding lipid shunting into non-oxidative pathways, which can ultimately disrupt normal cellular function leading to damaging effects of the heart.