Education

  • 2011 Postdoctoral Fellow, Sarah W. Stedman Nutrition & Metabolism Center, Duke University, Durham NC
  • 2005 PhD, Department of Physiology, East Carolina University, Greenville, NC
  • 1999 MA, Department of Exercise and Sport Science, East Carolina University, Greenville, NC
  • 1996 BS, Department of Exercise and Sport Science, Iowa State University, Ames, IA

Research Interests

Dr. Noland's general research interests lie in substrate metabolism in health and disease, with special interest in lipid metabolism in obesity, insulin resistance and diabetes.

He focuses primarily on assessing abnormalities in substrate utilization/switching in skeletal muscle; however, he has explored similar issues in heart, liver, and kidney to more fully understand the coordinated regulation/dysregulation of fuel utilization amongst various organ systems contributing to the pathogenesis of these metabolic diseases. Early projects focused on characterizing alterations in substrate metabolism in various models of disparate insulin sensitivity at the whole body level, as well as in isolated organelle preparations (mitochondria and peroxisomes), tissue homogenates, intact tissue strips, and cell culture models. Many of these investigations involved interventions intended to augment glucose tolerance, such as exercise training and pharmacotherapy, to identify potentially important mechanisms involved in restoring metabolic control.

Dr. Noland has recently investigated such mechanisms involved in skeletal muscle substrate handling using molecular physiology techniques, like recombinant adenovirus-mediated gene delivery and RNAi-mediated gene silencing, to manipulate gene expression in cell culture (rodent and human) and animal models. The use of cell culture, rodent, and human models to characterize and explore mechanisms involved in the regulation/dysregulation of fuel metabolism has provided comprehensive and informative results which will ultimately be used to determine logical pathways to target therapeutically in order to improve metabolic outcomes in human disease.

Department:  Skeletal Muscle Physiology Laboratory

Selected Publications

Peer Reviwed Journal Articles

  1. Linden, M.A., Burke, S.J., Pirzadah, H.A., Huang, T.Y., Batdorf, H.M., Mohammed, W.K., Jones, K.A., Ghosh, S., Campagna, S.R., Collier, J.J., and Noland, R.C. Pharmacological inhibition of lipolysis prevents adverse metabolic outcomes during glucocorticoid administration. Mol Metab. 2023 Aug. PMCID: PMC10300254.
  2. Huang, T.Y., Linden, M.A., Fuller, S.E., Goldsmith, F.R., Simon, J., Batdorf, H.M., Scott, M.C., Essajee, N.M., Brown, J.M., and Noland, R.C. Combined effects of a ketogenic diet and exercise training alter mitochondrial and peroxisomal substrate oxidative capacity in skeletal muscle. Am J Physiol Endocrinol Metab, 2021 Apr 12. PMCID: PMC8285595.
  3. Huang, T.Y., Goldsmith, F.R., Fuller, S.E., Simon, J., Batdorf, H.M., Scott, M.C., Essajee, N.M., Brown, J.M., Burk, D.H., Morrison, C.D., Burke, S.J., Collier, J.J., and Noland, R.C. Response of liver metabolic pathways to ketogenic diet and exercise are not additive. Med Sci Sports Exerc., 2020, Jan; 52(1): 37-48. PMCID: PMC6910928.
  4. Ghosh, S., Wicks, S.E., Vandanmagsar, B., Mendoza, T.M., Bayless, D.S., Salbaum, J.M., Dearth, S.P., Campagna, S.R., Mynatt, R.L., and Noland, R.C. Extensive metabolic remodeling after limiting mitochondrial lipid burden is consistent with an improved metabolic health profile. J. Biol. Chem. 2019, May 16. PMCID: PMC6699851. *Editor’s Choice
  5. Fuller, S.E., Huang, T.Y., Simon, J., Batdorf, H.M., Essajee, N.M., Scott, M.C., Waskom, C.M., Brown, J.M., Burke, S.J., Collier, J.J., and Noland, R.C. Low-intensity exercise induces acute shifts in liver and skeletal muscle substrate metabolism but not chronic adaptations in tissue oxidative capacity. J. Appl Physiol. 2019, Jul 1; 127(1): 143-156. PMCID: PMC6692746.
  6. Wicks, S.E., Vandanmagsar, B., Haynie, K.R., Fuller, S.E., Warfel, J.D., Stephens, J.M., Wang, M., Han, X., Zhang, J., Noland, R.C. and Mynatt, R.L. Impaired mitochondrial fat oxidation induces adaptive remodeling of muscle metabolism. Proc Natl Acad Sci USA, 2015 Jun 23: 112(25): E3300-9. PMCID: PMC4485116.
  7. Noland, R.C. Exercise and regulation of lipid metabolism. In: Progress in Molecular Biology and Translation Science: Molecular and Cellular Regulation of Adaptation to Exercise (vol 135). Bouchard C. (Ed), Academic Press, 39-74; 2015, July 31.
  8. Muoio, D.M.*‡, Noland, R.C.‡, Kovalik, J.P., Seiler, S.E., Davies, M.N., DeBalsi, K.L., Ilkayeva, O.R., Stevens, R.D., Kheterpal, I., Zhang, J., Covington, J.D., Bajpeyi, S., Ravussin, E., Kraus, W., Koves, T.R., and Mynatt, R.L.*  Muscle-specific deletion of carnitine acetyltransferase compromises glucose tolerance and metabolic flexibility.  Cell Metabolism, 2012 May 2: 15: 764-777.  (‡equal contribution, *co-corresponding authors).  PMCID: PMC3348515.
  9. Noland, R.C., Koves, T.R., Seiler, S.E., Lum, H., Lust, R.M., Ilkayeva, O.R., Stevens, R., Hegardt, F.G., and Muoio, D.M. Carnitine insufficiency caused by aging and overnutrition compromises mitochondrial performance and metabolic control. J Biol Chem, 2009 June 24.  PMCID: PMC2755692.
  10. Koves, T.R., Ussher, J.R., Noland, R.C., Slentz, D., Mosedale, M., Ilkayeva, O., Bain, J., Stevens, R., Dyck, J.R., Newgard, C.B., Lopaschuk, G.D., and Muoio, D.M.  Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance.  Cell Metabolism, 2008 Jan: 7(1): 45-56.  PMID: 18177724.
  11. Noland, R.C., Woodlief, T.L., Whitfield, B.R., Manning, S.M., Evans, J.R., Dudek, R.W., Lust, R.M., and Cortright, R.N. Peroxisomal-mitochondrial oxidation in a rodent model of obesity-associated insulin resistance. Am J Physiol Endocrinology & Metabolism, 2007 Oct: 293(4): E986-E1001.  PMID: 17638705.
  12. Noland, R.C., Thyfault, J.P., Henes, S.T., Whitfield, B.R., Woodlief, T.L., Evans, J.R., Lust, J.A., Britton, S.L., Koch, L.G., Cortright, R.N., and Lust, R.M.  Artificial selection for high-capacity endurance running is protective against the development of high fat diet-induced insulin resistance.  Am J Physiol Endocrinology & Metabolism, 2007 July: 293(1): E31-41.  PMID: 17341547.

PubMed Publications
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