Instructor of Medicine
Dr. Chakravarthy received his medical and doctoral degrees from the University of Texas Medical School and the M.D. Anderson Cancer Center at Houston in 2001 where he studied cell biology and physiology with Frank Booth (1997-2000). He was elected to the Medical Honors Society, Alpha Omega Alpha (ΑΩΑ), in 2001. He did his clinical training in internal medicine at the Hospital of the University of Pennsylvania (2001-2003) where he received the Maurice F. Attie Resident Teaching Award for excellence in teaching and patient care. He did his subspecialty training in endocrinology at Washington University School of Medicine and the Barnes-Jewish Hospital, where he also obtained his postdoctoral research training in integrative physiology with Clay Semenkovich (2003-2006). In recognition of his postdoctoral research he received the Endocrine Scholar Award from the Endocrine Society for outstanding basic science research in 2006, and is a recipient of the American Diabetes Association Junior Faculty Award (2007-2010). Dr. Chakravarthy joined the faculty in the Department of Medicine in 2006.
We are interested in understanding how adult metabolic diseases such as type 2 diabetes are programmed during intrauterine life. Epidemiological observations show a strong association between decreased birth weight and development of type 2 diabetes early in adulthood. However, the underlying mechanisms, including the fundamental question of how body size is determined remains poorly understood. Recently, we found that mice genetically engineered to have only half the normal activity of an enzyme called fatty acid synthase (FAS) — the critical enzyme responsible for the synthesis of new fatty acids from dietary glucose — have decreased intrauterine body size, and develop diabetes with age. Thus, FAS haploinsufficiency in a mouse model appears to recapitulate the human condition, thereby allowing us to examine the pathogenetic details of the developmental programming of diabetes. Combining biochemical techniques with classical physiology, we are identifying the molecular basis for the in utero programming of pancreatic beta cell mass and their subsequent failure. These findings can be translated to humans by identifying potential FAS gene polymorphisms in populations that may predict decreased intrauterine size and subsequent development of type 2 diabetes. Identifying these mechanisms could establish new strategies to prevent the developmental programming of type 2 diabetes.