Shawn C. Burgess
Education
1995 BS, Chemistry, The University of Texas at Dallas
1997 MS, Chemistry, The University of Texas at Dallas
2000 Doctorate, Chemistry, The University of Texas at Dallas
2003 Post-doctoral work, UTSW Medical Center
Academic Appointments
Assistant Professor, Advanced Imaging Center, UTSW Medical Center
Assistant Professor, (Secondary) Dept. of Pharmacology, UTSW Medical Center
Adjunct Assistant Professor, Dept. of Molecular and Cell Biol., The University of Texas at Dallas
Overview
Intermediary metabolism is the complex process by which nutrients are transformed into cellular building blocks, redistributed to specific cellular fuels, converted to storage molecules or oxidized to provide energy. Disorders of intermediary metabolism are the basis of many diseases, so techniques that allow quantitative measures of flux of molecules through these metabolic pathways are important tools for basic and clinical science. Nuclear Magnetic Resonance (NMR) spectroscopy in conjunction with stable isotope (non-radioactive) tracers is a powerful technique for understanding intermediary metabolism. NMR is especially informative about the chemical nature of an atom (and its neighboring atoms) in a molecule and thus provides enormous insight into the metabolic fate of isotope labeled tracers. Administration of stable isotope tracers, containing carbon-13 or deuterium, in humans or animals followed by NMR analysis of tissue or fluid extracts reveals the metabolic flux of a number of biochemical pathways. My interest is in using this technology to study hepatic energy production and gluconeogenesis in the liver and kidney. I have studied these pathways with collaborators with mouse models having specific defects in hepatic energy and glucose metabolism and have transitioned the information gained from animal studies towards the understanding of human physiology by partnering with clinicians who have human subjects with abnormal metabolic features such as obesity and diabetes. This powerful cross-disciplinary approach unites my interests in metabolism with molecular biologists and clinicians, providing an increasingly integrated picture of the physiology of metabolic diseases.
Select Publications
1. Burgess SC, Hausler N, Merritt M, Jeffrey FMH, Storey C, Milde A, Koshy S, Lindner J, Magnuson MA, Malloy CR, and Sherry AD. Impaired Tricarboxylic Acid Cycle Activity in Mouse Livers Lacking Cytosolic Phosphoenolpyruvate Carboxykinase. J Biol Chem 279: 48941-48949, 2004.
2. Burgess SC, Jeffrey FMH, Storey C, Milde A, Hausler N, Merritt M, Moulder H, Holm C, Sherry AD, Malloy CR. Effect of Murine Strain on Metabolic Pathways of Glucose Production after Brief or Prolonged Fasting. Am J Physiol Endocrinol Metab 289:E53-61, 2005.
3. Burgess SC, Leone TC, Wende AR, Croce MA, Chen Z, Sherry AD, Malloy CR, and Finck BN. Diminished hepatic gluconeogenesis via defects in tricarboxylic acid cycle flux in peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha)-deficient mice. J Biol Chem 281: 19000-19008, 2006.
4. Browning JD, Davis J, Saboorian MH, and Burgess SC. A low-carbohydrate diet rapidly and dramatically reduces intrahepatic triglyceride content. Hepatology 44: 487-488, 2006. 5. Burgess SC, He T, Yan Z, Lindner J, Sherry AD, Malloy CR, Browning JD, Magnuson MA. Cytosolic Phosphoenolpyruvate Carboxykinase Does Not Solely Control the Rate of Hepatic Gluconeogenesis in the Intact Mouse Liver. Cell Metabolism
5: 313-320, 2007. 6. SC Burgess, T Kitazume, K Iizuka, NH Jeoung, RA Harris, BC. Miller, Y Kashiwaya, RL. Veech and K Uyeda. Mechanisms for the Reduced NAD/NADH REDOX potential and lower energy state of liver of Carbohydrate response element-binding protein (ChREBP) deficient mice. JBC. In PRESS, 2008.
- Updated: December 12, 2008
