Rupangi Vasavada, PhD
Research Topics:Apoptosis/Cell Death, Diabetes, Growth, Growth Factors and Receptors, Insulin, Knockout Mice, Receptors, Regeneration, Signal Transduction, Transgenic Mice, Transplantation
Diabetes, a major metabolic disease, affects ~10% of the US population, with an expected growth rate of 20-33% by 2050, according to the CDC, causing one of the highest life expectancy and economic tolls to the health system. All forms of diabetes ultimately result from the loss of functional pancreatic beta cells that produce insulin. It is now known that even patients with long-term diabetes retain residual beta cells with the potential to proliferate and regenerate. Therefore, enhancing a patient’s own functional beta cell mass, through improved function, survival and/or proliferation of existing beta cells, or through the formation of new beta cells from precursor cells, represent potential future therapeutic approaches for the treatment of diabetes.
My lab has been interested in understanding the pathways and mechanisms that regulate beta cell growth, survival and function, with the ultimate objective being to enhance regeneration of functional beta cells in vivo. We have focused on the role of specific growth factors, parathyroid hormone-related protein (PTHrP), lactogens, and more recently, osteporotegerin (OPG), in normal beta cell physiology. We use transgenic overexpression as well as conditional knockout mouse models to determine the in vivo effects of these growth factors and their downstream signaling and molecular pathways on beta cell proliferation, survival and function.
The ultimate objective of our research is to find ways to enhance preservation and regeneration of functional beta cells in vivo, for the treatment of diabetes. There are several approaches we have taken towards this therapeutic goal. 1) To test the effects of acute and systemic administration of molecules in rodent models of depleted beta cell mass and in the pathophysiological settings of type 1 and type 2 diabetes. 2) To assess the effects of these molecules on human beta cells in vitro, and in vivo, in rodent models of islet transplantation. 3) More recently, we have focused attention on discovering ways to quantify human beta cell proliferation in collaboration with Dr. Garcia-Ocana. The currently used methods can label dividing cells but have not convincingly demonstrated an increase in beta cell numbers. As the ultimate goal in the treatment of diabetes is to increase human beta cell mass, we are developing a novel labeling tool to address this problem.
This work is currently funded by the NIH/NIDDK, and the Juvenile Diabetes Research Foundation.For a complete list of my publications, please visit the following link: http://www.ncbi.nlm.nih.gov/sites/myncbi/rupangi.vasavada.1/bibliography/41142260/public/?sort=date&direction=ascending