Patrick T. Fueger, PhD Assistant Professor, Department of Pediatrics
Assistant Professor: Department of Pediatrics Department of Cellular and Integrative Physiology
Research Group Website: Diabetes
Patrick T. Fueger, Ph.D., joined the Herman B Wells Center for Pediatric Research as principal investigator Feb.1 on the basic diabetes research team headed by Raghu Mirmira, M.D., Ph.D. Fueger has been a postdoctoral fellow from 2004 to 2009 at Duke University in the Department of Pharmacology and Cancer Biology and the Sarah W. Stedman Nutrition and Metabolism Center. He was recently published in 2008 in Molecular Endocrinology on the role of trefoil factor 3 in beta cell proliferation. His research expertise in pancreatic beta cells and islets adds to the knowledge base the diabetes research team has established so far.
Fueger received a National Institute of Health Pathway to Independence Award in 2007 for his work on mechanisms to induce islet proliferation. In 2005 he received the Juvenile Diabetes Research Foundation Postdoctoral Fellowship Award entitled "Role of histone deacetylases in beta-cell survival and function." He received his Ph.D. in 2004 from Vanderbilt University from the Department of Molecular Physiology & Biophysics and his M.S. in human kinetics and B.S. in biological sciences from the University of Wisconsin-Milwaukee.
A former Hoosier, Fueger is a board member of the Diabetes Youth Foundation of Indiana and has been the chair of the program committee from 1995-2006. He has also been active in the diabetes camp that the foundation established. Fueger has received numerous awards for his work in endocrinology and metabolism, and he is a professional member of the American Diabetes Association and the American Physiological Society.
Glucose homeostasis is primarily maintained by the intricate balance of the glucoregulatory, pancreatic hormones insulin and glucagon. Type 1 diabetes mellitus results from the autoimmune destruction of pancreatic beta cells which produce insulin. Currently, the only available cure for type 1 diabetes is pancreatic or islet transplantation. A primary limitation of these bona fide cures is the limited availability of pancreata and pancreatic islets from cadaver donors. Moreover, islet transplants are compromised by the rapid decline in beta cell mass that occurs immediately following transplantation. Because of this bottleneck in islet availability, much work has been performed with the goal of finding an alternative source of insulin-producing cells as well as establishing methods to stimulate proliferation of islets harvested for transplantation. The focus of my research program addresses the critical need to establish methods to increase functional pancreatic islet mass.
The projects currently being conducted in the laboratory are directed towards identifying novel beta growth factors, elucidating their signaling pathways, and translating these discoveries into animal transplantation and/or beta cell expansion models. In addition, we are attempting to minimize deficits in functional beta cell mass that occur in diabetes by abrogating cell death.