Peter Tontonoz
University of California, Los Angeles
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Primary Section: 42, Medical Physiology and Metabolism Secondary Section: 22, Cellular and Developmental Biology Membership Type:
Member
(elected 2020)
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Biosketch
Dr. Tontonoz is recognized for his work on cellular and systemic lipid metabolism. His laboratory has elucidated pathways for the regulation of lipid uptake, transport and efflux, and shown how these pathways impact the function of metabolic tissues and immune cells in physiology and disease. Dr. Tontonoz was born in Worcester, Massachusetts and grew up in Wilmington, Delaware. He received his B.A. from Wesleyan University in 1989 and his M.D. and Ph.D. from Harvard Medical School in 1996. He completed his residency training in pathology at the University of California, San Diego and a postdoctoral fellowship at the Salk Institute for Biological Studies. He joined the faculty of the University of California, Los Angeles in 1999. Dr. Tontonoz has been president of the American Society of Clinical Investigation and is a member of the National Academy of Sciences, the American Society of Clinical Investigation, and the Association of American Physicians.
Research Interests
The focus of Dr. Tontonoz’s laboratory is the control of gene expression by lipids and the role of nuclear receptors in metabolism. Obesity, diabetes and cardiovascular disease are the leading causes of morbidity and mortality in industrialized societies. The common thread that links these disorders is dysregulation of lipid metabolism. Dr. Tontonoz’s work has helped to reveal fundamental mechanisms by which animals maintain cellular and whole-body lipid homeostasis and how these pathways are perturbed in the setting of diseases such as atherosclerosis and diabetes. By studying transcriptional networks controlled by lipid-activated transcription factors, Tontonoz has elucidated pathways governing lipid uptake, transport and efflux. His work has helped to define how nuclear receptors coordintate the removal of excess cholesterol from cells such as macrophages, and how changes in cellular cholesterol metabolism can alter the function of innate and acquired immune cells. He also identified the E3 ubiqutin ligase Idol as a regulator of LDL metabolism and uncovered the key role of the Aster proteins in nonvesicular plasma membrane to ER cholesterol transport. A better understanding of fundamental regulatory strategies in metabolism may identify opportunities for therapeutic intervention in human metabolic disease.
