Mitochondria are known as the "engines" of the cell, converting metabolites into a useable form of energy for the rest of the cell. Overloading cells with fuel due to excess caloric intake and/or inactivity compromises mitochondrial function whereas exercise training enhances mitochondrial oxidative capacity. Research in my lab is directed at deciphering the molecular mechanisms governing mitochondrial bioenergetics and function in the context of the etiology of metabolic disease as well as disease prevention/treatment.
NIH RO1 DK073488 Mitochondrial Bioenergetics and Etiology of Insulin Resistance (04/30/11). The long term objective of this research is to determine if the loss of mitochondrial function and insulin sensitivity stem from a common metabolic disturbance, i.e., oxidative stress. The projects utilize a newly developed permeabilized fiber approach to study mitochondrial function in rodent skeletal muscle, pharmacological agents and transgenic models to manipulate mitochondrial ROS production and scavenging.
NIH RO1 DK074825 Linking Mitochondrial Bioenergetics to Muscle Insulin Sensitivity (01/31/14). This project examines the potential link between mitochondrial function/dysfunction and insulin sensitivity in 1) obese humans 2) younger subjects of normal weight and with normal insulin sensitivity acutely exposed to high caloric/high fat diet; and 3) in obese subjects undergoing a diet/exercise intervention to reverse insulin resistance.
2009– Director of Research, The Metabolic Institute for the Study of Diabetes and Obesity, East Carolina University, Greenville, NC
2006– Associate/Full Professor, Exercise and Sport Science and Department of Physiology, East Carolina University, Greenville, NC
1998–2006 Assistant/Associate Professor, Department of Physiology, Yale University, New Haven, CT
1996–2006 Assistant/Associate Fellow, John B. Pierce Laboratory, New Haven, CT
Education & Training
1993–1996 Post Doctoral Fellow, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX
1989– 1993 Ph.D. Biochemistry, East Carolina University School of Medicine,
1984–1986 M.S. Exercise Physiology, Human Performance Laboratory, Ball State University, Muncie, IN
1980–1984 B.S., Physical Education,
Anderson EJ, Kypson AP, Rodriguez E, Anderson CA, Lehr EJ, Neufer PD. Substrate-specific derangements in mitochondrial metabolism and redox balance in atrium of type 2 diabetic human heart. J. Am. Coll. Cardiol. (in press).
Anderson EJ, Lustig ME, Boyle KE, Woodlief TL, Kane DA, Lin C-T, Price JW III, Kang L, Rabinovitch PS, Szeto HH, Houmard JA, Cortright RN, Wasserman DH and Neufer PD. Mitochondrial H2O2 emission and cellular redox state link excess fat intake to insulin resistance in both rodents and humans. J. Clin. Invest. 119:565-574, 2009.
Anderson EJ, Yamasaki HA, and Neufer PD. Induction of endogenous UCP3 suppresses mitochondrial oxidant emission during fatty-acid supported respiration. J. Biol. Chem. 282:31257-31266, 2007.
Anderson EJ, and Neufer PD. Type II skeletal myofibers possess unique properties that potentiate mitochondrial H2O2 generation Am. J. Physiol.: Cell Physiology 290:C844-C851, 2006.