Implications of Apolipoprotein E Deficiency on Cardiac Mitochondrial Oxygen Consumption in a Young Mouse Model

ORIGINAL RESEARCH, November 2014, VOL III ISSUE I, ISSN 2042-4884
10.5083/ejcm.20424884.125 , Cite or Link Using DOI
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Cynthia Rocha, Celena Scheede-Bergdahl, Thomas Whitesell, Andreas Bergdahl

ABSTRACT

Background:
Apolipoprotein E (ApoE) is necessary for normal lipid metabolism. Deficiency of this protein hinders plasma clearance of both triglycerides and cholesterol. Lipids are, shunted through alternate metabolic pathways, thus resulting in abnormal mitochondrial function. Given the oxygen consumption required for normal heart function, the mitochondria are of particular importance and the preservation of their optimal function is critical.

Methods: Using high-resolution respirometry (HRR) and immunoblotting to quantify mitochondrial oxidative phosphorylation (OXPHOS) capacity in permeabilised cardiomyocytes, the goal of this study was to investigate the effects of ApoE deficiency on energy metabolism in the hearts of young mice.
Results: Our results demonstrate a reduced basal respiration (ADP restricted) in the ApoE-/- mice. This is furthermore translated to an increased efficiency of the mitochondria, as expressed by a higher respiratory control ratio in ApoE-/- mice.

Conclusions: This indicates that early stages of ApoE deficiency positively affects oxidation and phosphorylation coupling within cardiac mitochondria. Our findings provide important information regarding the early phases of preferential lipid metabolism in cardiomyocytes and can help explain the benefits of short term high fat intake for prevention of development and progression of heart failure.