Robert Noland, PhD
Skeletal Muscle Metabolism
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2011 Postdoctoral Fellow, Sarah W. Stedman Nutrition & Metabolism Center, Duke University, Durham NC
2005 Ph.D., Department of Physiology, East Carolina University, Greenville, NC
1999 M.A., Department of Exercise and Sport Science, East Carolina University, Greenville, NC
1996 B.S., Department of Exercise and Sport Science, Iowa State University, Ames, IAWebsite:http://cobre.pbrc.edu/projects-pis/robert-noland/default.asp
My general research interests lie in substrate metabolism in health and disease, with special interest in lipid metabolism in obesity, insulin resistance and diabetes. I have focused primarily on assessing abnormalities in substrate utilization/switching in skeletal muscle; however, I have 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. Recently I have begun investigating 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.
Peer Reviewed Journal Articles
1. Ruggiero, C., Elks, C.M., Kruger, C., Cleland, E., Addison, K. Noland, R.C. and Stadler, K. Albumin-bound fatty acids but not albumin itself alter redox balance in tubular epithelial cells and induce a peroxide-mediated redox-sensitive apoptosis. Am J Physiol Renal Physiol, 2014 Feb 5. PMID: 24500687.
2. Seiler, S.E., Martin, O.J., Noland, R.C., Slentz, D.H., DeBalsi, K.L., Ilkayeva, O.R., An, J., Newgard, C.B., Koves, T.R. and Muoio, D.M. Obesity and lipid stress inhibit carnitine acetyltransferase activity. J Lipid Res, 2014 Jan 6. PMID: 24395925.
3. 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). PMID: 22560225.
4. Arumugam, R., Horowitz, E., Noland, R.C., Lu, D., Fleenor, D., and Freemark, M. Regulation of Islet ß-Cell Pyruvate Metabolism Interactions of Prolactin, Glucose, and Dexamethasone. Endocrinology, 2010 May 19. PMID: 20484462.
5. Bikman, B.J., Woodlief, T.L., Noland, R.C., Britton, S.L., Koch, L.G., Lust, R.M., Dohm, G.L., and Cortright, R.N. High-fat diet induces IKKB and reduces insulin sensitivity in rats with low running capacity. Int J Sports Med, 2009 June 30. PMID: 19569009.
6. 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. PMID: 19553674.
7. Makowski, L., Noland, R.C., Koves, T.R., Xing, W., Ilkayeva, O.R., Muehlbauer, M.J., Stevens, R., and Muoio, D.M. Metabolic profiling of PPAR-/- mice reveals defects in carnitine and amino acid homeostasis that are partially reversed by oral carnitine supplementation. FASEB J, 2009 Feb: 23(2): 586-604. PMID: 18945875.
8. 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.
9. 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.
10. 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.
11. Gray, S.L., Dalla Nora, E., Backlund, E.C., Manieri, M., Virtue, S., Noland, R.C., O’Rahilly, S., Cortright, R.C., Cinti, S., Cannon, B., and Vidal-Puig, A. Decreased brown adipocyte recruitment and thermogenic capacity in mice with impaired peroxisome proliferators-activate receptor (P465L PPARgamma) function. Endocrinology, 2006 Dec: 147(12): 5708-14. PMID: 16980437.
12. Koves, T.R., Noland, R.C., Bates, A.L., Henes, S.T., Muoio, D.M., and Cortright, R.N. Subsarcolemmal and intermyofibrillar mitochondria play distinct roles in regulating skeletal muscle fatty acid metabolism. American Journal of Physiology: Cell Physiology, 2005, May: 288(5): C1074-82. PMID: 15647392.
13. Noland, R.C., Hickner, R.C., Jimenez-Linan, M., Vidal-Puig, A., Zheng, D., Dohm, G.L., and Cortright, R.N. Acute endurance exercise increases skeletal muscle UCP-3 gene expression in untrained but not trained humans. Metabolism, 2003 Feb: 52(2): 152-8. PMID: 12601624.
14. Noland, R.C., Baker, J.T., Boudreau, S.R., Kobe, R.W., Tanner, C.J., Hickner, R.C., McCammon, M.R., and Houmard, J.A. Effect of intense training on plasma leptin in male and female swimmers. Med Sci Sports Exerc. 2001 Feb: 33(2): 227-31. PMID: 11224810.
15. Brunson, M.A., Lombard, S., Mahar, M.T., Baker, J.T., Keen, S.U., Miller, L.R., Moreland, M.R., Noland, R.C., Williams, G., and McCammon, M.R. Cross-validation of five techniques to determine body composition. Med Sci Sports Exerc. 1998 May: 30(5) Supplement: 276.
1. Thyfault, J.P., Rector, R.S., and Noland, R.C. Metabolic inflexibility in skeletal muscle: a prelude to the cardiometabolic syndrome? J CardioMetabolic Syndrome, 2006 Summer: 1(3): 184-9. PMID: 17679820.