About the Lab
The incidence of diabetes mellitus has reached epidemic proportions worldwide. This debilitating disease greatly increases population morbidity and mortality and places a substantial burden on health care systems globally. For this reason, increased understanding of molecular and physiological mechanisms underlying induction of diabetes is essential for development of novel therapeutic and preventive approaches.
Pathophysiology of diabetes is complex; however, evidence suggests that pancreatic beta cell failure is a hallmark abnormality responsible for failed regulation of glucose homeostasis, induction of hyperglycemia and onset of numerous tissue complications. Specifically, a key feature precipitating the onset of hyperglycemia in both type 1 and type 2 diabetes is the induction of beta cell dysfunction and loss of beta cell numbers, collectively called beta cell mass. Whereas in type 1 diabetes, beta cell loss and dysfunction occur due to an autoimmune attack leading to near total ablation of beta cells. Cell loss and dysfunction is more gradual in patients with type 2 diabetes and occurs in the setting of environmental triggers, such as obesity. Thus, development of successful diabetes treatment strategies requires regeneration and restoration of appropriate beta cell numbers and function.
Current research in the Islet Regeneration Lab is focused on basic science and translational research into the pathophysiology of diabetes, with particular emphasis on understanding the role of gene-environment interaction in the regulation of pancreatic beta cell function, survival and regeneration. To accomplish these goals, the lab uses an integrative approach ranging from cellular, molecular and biochemical studies to in vivo physiology in genetic and environmental rodent models of diabetes and obesity. More recently, the focus of research has been on the role of circadian clock genes and the circadian system as a novel regulator of beta cell function and regeneration.
Over the years the lab has been funded by the National Institutes of Health (NIH), private foundations and the pharmaceutical industry and has published extensively in the areas of basic beta cell biology and physiology, molecular regulation of insulin secretion, and circadian control of beta cell function and turnover.