Dr. David J. Mangelsdorf received his BS in Biology and Chemistry from Northern Arizona University in Flagstaff (1981) and his PhD in Biochemistry from the University of Arizona in Tucson (1987). He did his postdoctoral studies at The Salk Institute for Biological Studies. Since 1993 he has been at UT Southwestern, where he currently is Professor and Chair of the Department of Pharmacology, and an Investigator of the Howard Hughes Medical Institute. He holds the Raymond and Ellen Willie Distinguished Chair in Molecular Neuropharmacology, in Honor of Harold B. Crasilneck, PhD and the Distinguished Chair in Pharmacology, and he is a member of the National Academy of Sciences.
Dr. Mangelsdorf’s research interests are focused on the mechanism of action of orphan nuclear receptors. Stemming from his early work with Ronald Evans at the Salk Institute and the discovery of RXR and its ligand (9-cis retinoic acid), his lab has since characterized ligands and physiologic functions for the LXRs, which bind oxysterols; FXR, which binds bile acids; and PPARs, which bind fatty acids. Together, these receptors govern nutrient metabolism during feeding and fasting, and they have become therapeutic targets for diseases such as atherosclerosis, cholestasis, and type 2 diabetes. Since 2003, Mangelsdorf has been working jointly with Dr. Steven Kliewer at UT Southwestern. The focus of their work has centered on two new nuclear receptor-initiated endocrine signaling pathways that govern feeding and fasting responses and are mediated by the fibroblast growth factors FGF19 and FGF21. Recently, their lab has also discovered the existence of an orthologous nuclear receptor pathway that is conserved in parasitic nematodes, and has shown that pharmacophores that target this pathway may represent a new class of vermicides.