Peter Light BiographyOffice / Clinic Information:
Edmonton, AB T6G 2E1
Phone: 780-492-3077 E-mail:
[email protected]
Scott Campbell (MSc student)
Kristian Jaeger (MSc student)
Nermeen Youssef (PhD student)
Chris Carter (Postdoctoral fellow)
Yi (Eva) Yu (Postdoctoral fellow)
Deepak Narang (PhD student) – co-supervisor
Scientific Focus: Current Research Interests: 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 fat metabolism. 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. Islet engineering 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. 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.
Publications: KATP channels KATP channels sit at the intracellular
crossroads between metabolism and cellular excitability, acting as
vital transducers of metabolic signals in many diverse cell types.
In this regard, my laboratory has made the following
contributions:
1. How intracellular esters of fat metabolism (acyl coenzyme As)
may control whole body glucose homeostasis (Nature 2008) and
activate the KATP channel complex (Metabolism, Molecular
Endocrinology, Endocrinology). 2. The properties, regulation and
pharmacology of cardiac and b cell KATP channels (J Physiol, BJP -
2 articles, FASEB J, PNAS, Diabetes, J Cardiovasc Pharmacol, J Mol
Endocrinology, Molecular Endocrinology, JBC, J Physiol). 3. KATP
channels containing common type 2 diabetes (T2D) susceptibility
genetic variants (Diabetes - 3 articles, Human Genetics).
Collectively, these studies have increased our current
understanding of the following: The mechanisms by which cardiac
cell dysfunction occurs and can be protected against during
ischemia/reperfusion injury; Why chronic elevation of intracellular
fats, that occurs in obesity, may affect some individuals more than
others in triggering type 2 diabetes; Novel pharmacogenomic
approaches for the improved treatment of T2D.
NCX1 NCX1 is a key membrane protein that is involved in the
maintenance of intracellular calcium homeostasis in many tissues
including the heart and endocrine pancreas. We have been
investigating the metabolic regulation and pharmacology of NCX1
with respect to cardiac ischemia reperfusion injury and the control
of endocrine hormones involved in glucose homeostasis. These
continuing studies have made the following contributions: 4. The
metabolic and molecular regulation of NCX1 (EMBO J, Molecular
Endocrinlogy, JMCC) and potential new avenues to improve cardiac
function after elective surgery (J Physiol, BJP, FASEB J) 5. NCX1
pharmacology and the development of glucose-sensitive
insulinotropic drugs for T2D (Diabetes 2009.