Robert Noland

Biography

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, IA

Research Interest

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.