Department of Biological Sciences

School of Natural Sciences and Mathematics

Faculty and Research

Shawn C. Burgess

Education

1995 BS, Chemistry, University of Texas at Dallas
1997 MS, Chemistry, University of Texas at Dallas
2000 Doctorate, Chemistry, University of Texas at Dallas
2003 Post-doctoral work, UTSW Medical Center

Academic Appointments

Associate Professor, (tenured) Advanced Imaging Center, UT Southwestern Medical Center
Associate Professor, (Secondary) Dept. of Pharmacology, UT Southwestern Medical Center
Division Chief, Division of Metabolic Mechanisms of Disease, AIRC, UT Southwestern Medical Center, Dallas
Adjunct Assistant Professor, Dept. of Molecular and Cell Biol., University of Texas at Dallas

Overview

Mammalian physiology requires extraordinary metabolic flexibility in order to adapt to normal variations in nutrient availability and energy requirements. This regulation is executed through hormone signaling, enzyme expression/modification and substrate level factors that control the rates of certain biochemical reactions, or metabolic flux. Ultimately, it is the dysregulation of metabolic flux that results in the manifestation of disease. The Burgess lab uses Nuclear Magnetic Resonance (NMR) spectroscopy and Mass Spectrometry (MS) in combination with stable isotope (non-radioactive) tracers to study the function of metabolism in disease or targeted interventions.  These quantitative approaches are joined with classic biomolecular methods, gene altered animal and cell models to investigate metabolic mechanisms of disease.  We focus mainly on pathways of lipid and carbohydrate metabolism in the context of obesity, insulin resistance and diabetes or in models with targeted alterations in hepatic energy and carbohydrate metabolism. The technologies and metabolic insight from this basic science approaches are then translated to human physiology and disease. Our goal is to use state of the art quantitative approaches to uncover the molecular and metabolic basis of disease.  See also: http://www.utsouthwestern.edu/labs/burgess/

Select Publications

  • Potthoff MJ, Potts A, He T, Duarte JAG, Taussig R, Mangelsdorf DJ, Kliewer SA, and Burgess SC. Colesevelam suppresses hepatic glycogenolysis by TGR5-mediated induction of GLP-1 action in DIO mice. American Journal of Physiology - Gastrointestinal and Liver Physiology 304: G371-G380, 2013.
  • Duarte JA, Carvalho F, Pearson M, Horton JD, Browning JD, Jones JG, Burgess SC. A high-fat diet suppresses de novo lipogenesis and desaturation but not elongation and triglyceride synthesis in mice. Journal of lipid research. 2014;55(12):2541-53.
  • McCommis KS, Chen Z, Fu X, McDonald WG, Colca JR, Kletzien RF, Burgess SC, Finck BN. Loss of Mitochondrial Pyruvate Carrier 2 in the Liver Leads to Defects in Gluconeogenesis and Compensation via Pyruvate-Alanine Cycling. Cell Metab. 2015;22(4):682-94.
  • Satapati S, Kucejova B, Duarte JA, Fletcher JA, Reynolds L, Sunny NE, He T, Nair LA, Livingston K, Fu X, Merritt ME, Sherry AD, Malloy CR, Shelton JM, Lambert J, Parks EJ, Corbin I, Magnuson MA, Browning JD, Burgess SC. Mitochondrial metabolism mediates oxidative stress and inflammation in fatty liver. J Clin Invest. 2015;125(12):4447-62.
  • Kucejova B, Duarte J, Satapati S, Fu X, Ilkayeva O, Newgard CB, Brugarolas J, Burgess SC. Hepatic mTORC1 Opposes Impaired Insulin Action to Control Mitochondrial Metabolism in Obesity. Cell Rep. 2016;16(2):508-19.

See also: http://www.ncbi.nlm.nih.gov/sites/myncbi/shawn.burgess.1/

  • Updated: November 14, 2016