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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.
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.