Kamat (nee Bhakta), Amrita

School of Medicine
Medicine
(210) 617-5197
kamat@uthscsa.edu

Dr. Amrita Kamat is an Associate Professor in the Department of Medicine at the University of Texas Health Science Center at San Antonio. She is also the Deputy Associate Chief of Staff for Research and Development at the Audie Murphy VA Hospital, South Texas Veterans Health Care System (STVHCS). Dr. Kamat has been associated with the Geriatric Research, Education and Clinical Center, STVHCS as a Research Health Scientist since 2003. She is a member of the Endocrine Society and Women in Endocrinology, and on the editorial board of Endocrine Research. She is a recipient of several professional honors and research grant awards. Dr. Kamat is serving on various committees at the University (eg. the SOM Faculty Diversity Committee) and the VA.

The primary focus of Dr. Kamat`s research is to understand the regulation of glucose and lipid metabolism during aging and fetal development, with particular emphasis on beta-adrenergic receptor mediated mechanisms in the liver. Novel findings from her laboratory suggest that increased hepatic beta-adrenergic receptor signaling augments lipid accumulation and induces insulin resistance in the liver. The two major projects currently running in her laboratory are: 1) Lipid metabolism and steatosis in liver. The goal of this project is to understand the pathogenetic mechanisms involved in excessive hepatic lipid accumulation (hepatic steatosis), a hallmark of nonalcoholic fatty liver disease. Her studies were the first to suggest that augmented beta-adrenergic receptor signaling leads to increased fat accumulation in the liver and 2) Developmental programming and type 2 diabetes. The goal of this project is to understand how developmental programming results in a predisposition to diabetes in humans. Specifically, this study is designed to determine whether increased exposure of fetal baboon hepatocytes to glucocorticoids in vivo during intrauterine growth restriction (IUGR) induces hepatic phosphoenolpyruvate carboxykinase (PEPCK) and glucose production via premature upregulation of beta2-adrenergic receptor and hepatocyte nuclear factor 4I?. These studies are being performed using cultured fetal baboon hepatocytes that retain their in vivo phenotype thus providing powerful in vitro tools to investigate mechanisms that regulate normal and programmed hepatic function. To our knowledge, it is the first time that nonhuman primate fetal hepatocytes have been isolated and cultured. Studies are also designed to determine if the increase in PEPCK and hepatic glucose production persists through puberty. IUGR and increased PEPCK transcription leading to augmented gluconeogenesis have been linked to the development of type 2 diabetes.