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Brody School of Medicine
Department of Physiology


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Dr. Ronald N. Cortright, Ph.D.
Ronald Cortright  Professor
Department of Exercise and Sport Science
School of Health and Human Performance
Department of Physiology

Office Phone: (252)737-4678
Lab: (252)744-2934
E-Mail: cortrightr@ecu.edu

Mailing Address:
Brody School of Medicine
East Carolina University
Greenville, NC 27858
 

 
Education
1978 B.A., Biology Hiram College, Hiram, OH
1989 M.A., Exercise Physiology Kent State University, Kent, OH
1995 Ph.D., Exercise Physiology Kent State University, Kent, OH
1995-1998 Post-doctoral Fellow Biochemistry, East Carolina University, Greenville, NC
 

 
Research Interests
The focus of the Cortright laboratory is to better understand cellular bioenergetics and metabolism, with emphasis on skeletal muscle, in order to develop strategies to treat obesity and type II diabetes. In this regard, studies examining the effects of exercise on mitocohdrial bioenergetics and substrate utlization are employed. Technologies examining mitochondrial respiration, genomics and prteomics are used. Models involving cell culture of human myotubes, in vitro assessments of human and rodent skeletal muscle biopsies, and free living animals and humans are utilized in experimental designs.
 
Current Research and Funding
2011-2012
Principle Investigator – Cortright, R.N. East Carolina Diabetes Obesity Research Institute. Impaired Mitochondrial Function in Skeletal Muscle of African-American vs. Caucasian Women.
Obesity and diabetes is also more than twice as prevalent among African-American women (AAW) than among Caucasian women (CW) in the United States (CDC Report 2011,9). Based on recent findings from our lab (8,14), we hypothesize that skeletal muscle mitochondrial function is altered in AAW vs. CW leading to reduced respiratory capacity, elevated free radical production/oxidative stress, and a greater propensity to develop obesity, insulin resistance, and diabetes. Using state-of-the-art permeabilized muscle fiber techniques, the proposed studies will address this hypothesis by focusing on two aspects of mitochondrial function: 1) control of basal (state 4) and ADP-stimulated (state 3) respiration, and 2) control of mitochondrial reactive oxygen species (ROS) emission.

2006-2011
Principle Investigator – Cortright, R.N. National Institutes of Health (1RO1DK075880-01) Impaired Acyl-CoA Synthetase-Muscle Lipid Oxidation in African American Women (AAW).
The purpose of this research is to determine if the impairment in skeletal muscle fat oxidation in African-American Women (AAW) is due to a defect in acyl-CoA synthetase (ACC), the enzyme required for activating fatty acids prior to transport and oxidation in the mitochondria and whether AAW will respond to exercise training by increasing the capacity of skeletal muscle to oxidize lipids, due in part to a normalization of ACS activity.
 
Recently Completed Projects
Principle Investigator – Cortright, R.N. National Institutes of Health (1RO1DK075880) Impaired Acyl-CoA Synthetase-Muscle Lipid Oxidation in African American Women (AAW). Funded September 2006 – 2010.
We hypothesize that the impairment in skeletal muscle fat oxidation in AAW is due to a defect in acyl-CoA synthetase, the enzyme required for activating fatty acids prior to transport and oxidation in the mitochondria. This defect likely contributes to the greater incidence of obesity and diabetes in this racial group of women. However, in lean CW, endurance exercise training stimulates the muscle's capacity to oxidize long-chain fatty acids. Our secondary hypothesis is that AAW will respond to endurance exercise training by increasing the capacity of skeletal muscle to oxidize lipids, due in part to a normalization of ACS activity. Additional recent experiments suggest a greater propensity for African-American women to generate reactive oxygen species which are linked to skeletal muscle insulin resistance. Mechanisms related to mitochondrial proton conductance are being explored including racial differences in uncoupling protein activity and the adenine nucleotide translocase antiporter (ANT1).

Principle Investigator - Cortright, R.N. National Institutes of Health (1 R15 DK061314-01). “Mitochondrial-Peroxisomal Fatty Acid Oxidation in Obesity.” Funded, September 15, 2003 - 2008.
The purpose of this research was to establish a role for peroxisomes in facilitating the oxidation of long-chain fatty acids by skeletal muscle mitochondria in the obese state. Results suggest a bioenergetic interaction between peroxisomal beta-oxidation and enhanced mitocohndrial oxidation of fatty acids. This suggests a possible target for therapeutic inteventions.

Principle Investigator - Cortright, R.N.
National Institutes of Health (1 R21 DK065183). “Dysregulation of Fatty-Acid Metabolism in Skeletal Muscle in African-American and Caucasian Women.” Funded, September, 2003 - 2008.
The purpose of this research was to identify the cellular sites of dysregulated fatty acid oxidation in the skeletal muscle of African American vs. Caucasian women. Results indicated a mitochondrial deficiency in lipid oxidation, predisposing this group to increased risk for obesity and diabetes. However, endurance exercise training rescued this deficiency, suggesting the need for regular exercise to reduce the risk for obesity and type II diabetes.
 
Recent Publications
Kane DA, Lin CT, Anderson EJ, Kwak HB, Cox JH, Brophy PM, Hickner RC, Neufer PD, Cortright RN. Progesterone Increases Skeletal Muscle Mitochondrial H2O2 Emission in Non-Menopausal Women. Am J Physiol Endocrinol Metab. 2011 Mar;300(3):E528-35.

Kane DA, Anderson EJ, Price JW 3rd, Woodlief TL, Lin CT, Bikman BT, Cortright RN, Neufer PD. Metformin selectively attenuates mitochondrial H2O2 emission without affecting respiratory capacity in skeletal muscle of obese rats. Free Radic Biol Med. 2010 Sep 15;49(6):1082-7.

Benjamin T. Bikman, Donghai Zheng, Daniel A. Kane, Ethan J. Anderson, Tracey L. Woodlief, Jesse W. Price, G. Lynis Dohm, P. Darrell Neufer, Ronald N. Cortright. Metformin Improves Skeletal Muscle Insulin Signaling Via Altered Ampk-Ikkb Activity In Obese Rats in a Fiber-Type Dependent Manner. (Int. J. Obesity, 2010).

Benjamin T. Bikman, Tracey L. Woodlief, Robert C. Noland, Steven L. Britton,  Lauren G. Koch, Robert M. Lust, G. Lynis Dohm, Ronald N. Cortright. Insulin Signaling in Rats with Low Running Capacity. Int. J. Sports Medicine, 30:631-635,  2009.

Ethan J. Anderson, Mary E. Conniff, Kristen E. Boyle, Tracey L. Woodlief, Daniel A. Kane, Chien-Te Lin, Jesse W. Price, III, Li Kang, Peter S. Rabinovitch, Hazel H. Szeto,Joseph A. Houmard, Ronald N. Cortright, David H. Wasserman, and P. Darrell Neufer. Mitochondrial H2O2 emission and cellular redox state link excess fat intake to insulin resistance. J. Clin. Invest. 2009 Feb 2. pii: 37048. doi: 10.1172/JCI37048. [Epub ahead of print].
 
Recent Scientific Presentations
  1. Evidence for High Fat Diet Induced Peroxisomal Activity in Skeletal Muscle from Low (LCR) and High (HCR) Capacity Endurance Running Rats. Ronald Cortright, Robert Noland1, Tracey Woodlief, Hyo-Bum Kwak, Jesse Price, Steven Britton, Lauren Koch, Robert Lust. The Integrative Biology of Exercise, Hilton-Head, Sept. 24-27, 2008.
  2. Medium Chain Fatty Acid Oxidation is Carnitine-Dependent and is Inhibited by Malonyl-CoA in Human Skeletal Muscle. Donghai Zheng, Daniel A. Kane, Tracey L. Woodlief, Julie H. Cox, Robert C. Hickner,G. Lynis Dohm, and Ronald N. Cortright. Diabetes, 58 (1): A363, 2009.
  3. Fractional Mitochondrial H2O2 Emission is Greater During Glycerophosphate-Versus Succinate- Supported Respiration in Human Skeletal Muscle. Daniel A. Kane, Julie Cox, Robert C. Hickner, Ronald N. Cortright, P. Darrell Neufer. Diabetes, 58(1): A391, 2009.
  4. Ten Days of Exercise Training Increases Fatty Acid- Supported Basal Respiration and Reduces Mitochondrial H2O2 Emission in Human Skeletal Muscle. Daniel A. Kane, Julie H. Cox, Robert C. Hickner, P. Darrell Neufer, Ronald N. Cortright. Diabetes, 58(1): A289, 2009.
  5. Simvastatin Impairs ADP-Stimulated Mitochondrial Respiration and Alters Apoptotic Signaling and Morphology in Human Skeletal Myotubes. Hyo-Bum Kwak, Anna Thalacker-Mercer, Ethan J. Anderson, Kristen E. Boyle, Joseph A. Houmard, Ronald C. Cortright, Marcas M. Bamman, and P. Darrell Neufer.  Diabetes, 58(1): A393, 2009.
  6. Hyo-Bum Kwak, Tracey L. Woodlief, Thomas D. Green, Julie H. Cox, Robert C. Hickner, P. Darrell Neufer, and Ronald N. Cortright. Overexpression of Long Chain Acyl-CoA Synthetase 5 Increases Fatty Acid Oxidation, While Altering Insulin Signaling in Primary Human Skeletal Myotubes. Diabetes 59: A670, 2010. 
  7. ACSM's Conference on Integrative Physiology of Exercise
  8. "Simvastatin increases mitochondrial oxidative stress and reduces Ca2+ retention capacity in human skeletal myotubes" Annual Meeting of the American College of Sports Medicine, CSM's Conference on Integrative Physiology of Exercise.  Miami Beach, September 22-25, 2010.
  9. 2011 Annual Meeting for Experimental Biology, Washington, DC, April 9-13, 2011. Spare Me the Lecture!. Ronald N. Cortright, Heidi L. Lujan, and Stephen E. DiCarlo. Departments of Exercise and Sport Science and Physiology.
  10. 2011 Annual Meeting for Experimental Biology, Washington, DC, April 9-13, 2011. Overexpression of Long Chain Acyl-CoA Synthetase 1 Increases Fatty Acid Oxidation in Primary Human Skeletal Myotubes. Hyo-Bum Kwak2,4, Tracey L. Woodlief1,4, Thomas D. Green2, Julie H. Cox1, Robert C. Hickner1,3,4, P. Darrell Neufer1,3,4, and Ronald N. Cortright1,3,4  1Exercise and Sport Science, 2Internal Medicine, 3Physiology, and the 4Diabetes and Obesity Institute, East Carolina University, Greenville, NC.