Peter Light at the IACS meeting, Hungary, October 2014
Dr. Light completed his PhD at the University of Birmingham, United Kingdom, and his post-doctoral training in Canada at the University of Calgary and University of Ottawa. In 1996 he decided to make Canada home when he joined the University of Calgary as Adjunct Professor of Pharmacology. In 2000 Dr. Light was recruited to the University of Alberta where he joined the Department of Pharmacology in the Faculty of Medicine and Dentistry. Dr. Light has advanced to the level of full Professor in the Department of Pharmacology and in July of 2010 he was appointed Director of the Alberta Diabetes Institute and Dr. Charles A. Allard Chair in Diabetes Research at the University of Alberta.
Islet signaling and diabetes
My laboratory studies the ionic events that control insulin secretion and how dysfunction can lead to impaired/incorrect insulin secretion contributing to the development of type 2 diabetes. In pancreatic beta-cells, hormonal and metabolic control of ion channel and exchanger function is crucial in transducing the correct insulin secretory response. We are studying the links between common genetic variations in the ATP-sensitive potassium channel in relation to beta-cell function, metabolism and pharmacogenomics. In addition, we are also investigating the potential for development of novel "glucose-sensitive" therapeutic agents that target ion transport processes within the beta-cell and intestinal L-cells.
The "Edmonton Protocol" has now become the gold standard for islet transplantation. However, there is still a clear need to improve both the longevity and function of the islet grafts. My lab is using molecular and gene delivery techniques in the in vitro donor islets to facilitate islet graft survival and insulin secretory capacity.
My lab is currently utilizing optogenetic techniques to engineer non-neuronal cells to secrete bioactive peptide hormones in a controllable manner.
Cardiac ischemia reperfusion injury
Our continuing studies on cardiac tissue have direct implications for the reversible (arrhythmias and stunning) and irreversible (necrosis/apoptosis) damage that occurs during myocardial ischemia/reperfusion (IR) injury. In this regard, it is a current focus of my laboratory’s research program to provide important new information on the cellular ionic events that occur during IR injury and identify mechanisms that may be harnessed to reduce myocardial damage. Specifically we are studying the roles of ATP-sensitive potassium channels and sodium/calcium exchangers (NCX1) in the etiology of IR injury, cardiac surgery and transplantation.