Associate Professor, CMMB Director of Graduate Studies
Office: BSF 206
Lab: BSF 238, 240
- B.S., College of New Jersey, Biology, 1993
- M.S., Clemson University, Microbiology, 1996
- Ph.D., University of Florida, Biomedical Sciences, 2001
Adjunct Professor, Burlington County College, 2010
Senior Research Associate, Children's Hospital of Philadelphia, 2006-2011
Post-Doc, University of Pennsylvania, 2003-2006
My position at USF is interdisciplinary and encompasses CMMB, Pediatric Epidemiological Center (PEC), and the Diabetes Center (DC). Therefore, my laboratory has broad based investigations relating to my own interests stemming from my studies at Children’s Hospital of Philadelphia (CHOP) and University of Pennsylvania in addition to collaborations with both the PEC and DC. These interests include type 1 diabetes and a novel hormone known as PANcreatic-DERived factor (PANDER).
Diabetes (type 1 and 2) is a serious lifelong disease that impacts health globally. Diabetes (mainly type 2) currently affects 246 million people worldwide and is expected to affect 380 million by 2025. Incidence of type 1 diabetes (T1D) has been increasing 3-5% per year, doubling every 20 years. With no cure, there is an urgent need for complete elucidation of this disease process. In collaboration with the PEC and DC, my laboratory seeks to identify the genetic, nutritional, and immunological factors involved in T1D. This is being performed in conjunction with a large-scale international study known as The Environmental Determinants of Diabetes in the Young (TEDDY), whereby we have enrolled approximately 8000 patients with known risk factors for development of T1D. Multiple biological specimens have been accumulated from these patients and analysis is underway to unravel critical clues toward understanding the onset of T1D.
In addition, my laboratory is investigating a novel hormone known as PANDER. Research arising from my appointment as a Senior Research Associate at CHOP provided some of the first evidence of the pleiotropic role of this molecule in regulating glycemic levels via both interaction with the pancreatic ß-cells and the liver. PANDER knockout mice have impaired glucose tolerance due to inhibited insulin secretion due to abnormal calcium handling. Interestingly, these mice also display decreased hepatic glucose production and gluconeogenic gene expression during fasting conditions (Diabetes, 2010:59(9):2209-18). Furthermore, our acute and transgenic models reveal that PANDER induces hepatic glucose production and results in abnormal glucose tolerance post-prandially and fasting (Endocrinology, 151(11):5174-84). One of the major abnormalities with type 2 diabetes (T2D) is increased hepatic glucose production, therefore, the significance of this research is that PANDER represents a potential molecule that may impact T2D based on the biological effect that PANDER has on target tissues involved in glucose regulation. The precise mechanism of action of PANDER in the pancreatic islets and liver is unknown and is an active area of research in my group.