Dr. Mary Ellen Harper, PhD

My laboratory in the Faculty of Medicine has a longstanding history (17 years) of research in the area of metabolic biochemistry and obesity. My career's research has resulted in 103 peer-reviewed papers to-date, some of which have been published in Nature, Nature Medicine, Cell Metabolism, PNAS, and FASEB J. I have attained the rank of Full Professor. Much of the research in my lab focuses on muscle mitochondrial energetics. We first established that mitochondrial energy conversion is more efficient (i.e., energy is conserved) in muscle from obese individuals who lose weight very slowly compared to individuals who lose weight very quickly in a clinical weight loss program (Harper et al, 2002). Specifically, we found that muscle mitochondrial proton leak is lower in diet-resistant individuals versus diet-sensitive individuals. Gene expression profiles in muscle and in whole blood are consistent with profound differences in oxidative phosphorylation and metabolic signaling pathways between these patient groups and in comparison to lean controls (Gerrits et al, 2010; Ghosh et al, 2011). Diet-sensitive individuals have higher proportions of type I and lower IIa fibers in vastus lateralis than diet-resistant individuals (Gerrits et al, 2010). Our recent findings show that leak in muscle is in part controlled by reversible modification of uncoupling protein 3 (UCP3) by glutathione (Mailloux et al, 2011). UCP2 is also controlled similarly by glutathionylation, and this affects glucose-stimulated insulin secretion (Mailloux et al, 2012).