Deborah Marie Muoio, PhD


Associate Professor in Medicine
Associate Professor in Pharmacology & Cancer Biology
Department / Division:
Medicine / Medicine-Endocrinology and Metabolism
Address:
4321 Medical Park Dr
Durham, NC 27704
Office Telephone:
(919) 479-2328
Training:
  • PhD, University of North Carolina at Chapel Hill, 1999
Research Interests:
Dr. Deborah Muoio is an Associate Professor in the Sarah. W. Stedman Nutrition and Metabolism Center, with appointments in the Departments of Medicine and Pharmacology & Cancer Biology. Her laboratory investigates mechanisms of metabolic regulation in skeletal muscle, with emphasis on molecular events that link overnutrition and inactivity to the development of insulin resistance. Her program features a multidisciplinary approach that combines integrative physiology and intermediary metabolism with cellular and molecular biochemistry, using model systems that range from primary human myocytes to genetically engineered mice. Recent studies by her research team have employed mass spectrometry-based metabolomics as a tool to understand the interplay between mitochondrial energetics and insulin action. Emergent findings from this work suggest that obesity-associated glucose intolerance stems from excessive β-oxidation and lipid-induced mitochondrial stress. Ongoing studies seek to identify signaling mechanisms that mediate crosstalk between muscle mitochondria and glucose regulatory pathways, with the goal of realizing new therapeutic opportunities for treating metabolic diseases. Three main project areas of her laboratory include: 1) mechanisms that link lipid oversupply to mitochondrial malfunction and insulin resistance in skeletal muscle, 2) mechanisms through which exercise enhances mitochondrial function, lipid tolerance and insulin sensitivity, and 3) translational studies to examine the impact of diet and/or exercise interventions on metabolic regulation and mitochondrial function in human skeletal muscle. This research is supported by grants from the NIH and the American Diabetes Association.
Representative Publications:
  • Makowski, L; Noland, RC; Koves, TR; Xing, W; Ilkayeva, OR; Muehlbauer, MJ; Stevens, RD; Muoio, DM. Metabolic profiling of PPARalpha-/- mice reveals defects in carnitine and amino acid homeostasis that are partially reversed by oral carnitine supplementation. The FASEB Journal. 2009;23:586-604.  Abstract
  • Koves, TR; Ussher, JR; Noland, RC; Slentz, D; Mosedale, M; Ilkayeva, O; Bain, J; Stevens, R; Dyck, JR; Newgard, CB; Lopaschuk, GD; Muoio, DM. Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance. Cell Metabolism. 2008;7:45-56.  Abstract
  • Muoio, DM; Newgard, CB. Fatty acid oxidation and insulin action: when less is more. Diabetes. 2008;57:1455-1456.  Abstract
  • Muoio, DM; Newgard, CB. Mechanisms of disease: molecular and metabolic mechanisms of insulin resistance and beta-cell failure in type 2 diabetes. Nature Reviews: Molecular Cell Biology. 2008;9:193-205.  Abstract
  • Muoio, DM. TXNIP links redox circuitry to glucose control. Cell Metabolism. 2007;5:412-414.  Abstract
  • Power, RA; Hulver, MW; Zhang, JY; Dubois, J; Marchand, RM; Ilkayeva, O; Muoio, DM; Mynatt, RL. Carnitine revisited: potential use as adjunctive treatment in diabetes. Diabetologia. 2007;50:824-832.  Abstract
  • Thyfault, JP; Cree, MG; Zheng, D; Zwetsloot, JJ; Tapscott, EB; Koves, TR; Ilkayeva, O; Wolfe, RR; Muoio, DM; Dohm, GL. Contraction of insulin-resistant muscle normalizes insulin action in association with increased mitochondrial activity and fatty acid catabolism. American Journal of Physiology: Cell Physiology. 2007;292:C729-C739.  Abstract
  • Gaillard, S; Grasfeder, LL; Haeffele, CL; Lobenhofer, EK; Chu, TM; Wolfinger, R; Kazmin, D; Koves, TR; Muoio, DM; Chang, CY; McDonnell, DP. Receptor-selective coactivators as tools to define the biology of specific receptor-coactivator pairs. Molecular Cell. 2006;24:797-803.  Abstract
  • Berggren, JR; Tanner, CJ; Koves, TR; Muoio, DM; Houmard, JA. Glucose uptake in muscle cell cultures from endurance-trained men. Medicine and Science in Sports and Exercise. 2005;37:579-584.  Abstract
  • Hammond, LE; Neschen, S; Romanelli, AJ; Cline, GW; Ilkayeva, OR; Shulman, GI; Muoio, DM; Coleman, RA. Mitochondrial glycerol-3-phosphate acyltransferase-1 is essential in liver for the metabolism of excess acyl-CoAs. Journal of Biological Chemistry. 2005;280:25629-25636.  Abstract
  • Hulver, MW; Berggren, JR; Carper, MJ; Miyazaki, M; Ntambi, JM; Hoffman, EP; Thyfault, JP; Stevens, R; Dohm, GL; Houmard, JA; Muoio, DM. Elevated stearoyl-CoA desaturase-1 expression in skeletal muscle contributes to abnormal fatty acid partitioning in obese humans. Cell Metabolism. 2005;2:251-261.  Abstract
  • Koves, TR; Li, P; An, J; Akimoto, T; Slentz, D; Ilkayeva, O; Dohm, GL; Yan, Z; Newgard, CB; Muoio, DM. Peroxisome proliferator-activated receptor-gamma co-activator 1alpha-mediated metabolic remodeling of skeletal myocytes mimics exercise training and reverses lipid-induced mitochondrial inefficiency. Journal of Biological Chemistry. 2005;280:33588-33598.  Abstract
  • Koves, TR; Noland, RC; Bates, AL; Henes, ST; Muoio, DM; Cortright, RN. Subsarcolemmal and intermyofibrillar mitochondria play distinct roles in regulating skeletal muscle fatty acid metabolism. American Journal of Physiology: Cell Physiology. 2005;288:C1074-C1082.  Abstract
  • An, J; Muoio, DM; Shiota, M; Fujimoto, Y; Cline, GW; Shulman, GI; Koves, TR; Stevens, R; Millington, D; Newgard, CB. Hepatic expression of malonyl-CoA decarboxylase reverses muscle, liver and whole-animal insulin resistance. Nature Medicine. 2004;10:268-274.  Abstract
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