Dr Peter Light
Full Professor, 2010-present.
Director of the Alberta Diabetes Institute.
Dr. Charles A. Allard Chair in Diabetes Research
BSc–Honours (Biological Sciences/Cell Physiology), University of Birmingham, UK, 1986
PhD (Biological Sciences/Cell Physiology), University of Birmingham, UK,1990
Teaching: PMCOL 371, PMCOL 512, PHARM367, PMCOL301/401/498,
Research: Molecular Pharmacology and New Therapeutics For Diabetes and Heart Disease
Research Interests / Laboratory Techniques
The research laboratory of Dr. Peter Light is located in the Alberta Diabetes Institute, University of Alberta. His lab researches ion transport processes controlling cellular excitability, utilizing a combination of electrophysiological, live-cell imaging, biochemical and molecular techniques to study the biophysics, physiology and pharmacology of ion channels and exchangers at the molecular, cellular, organ and whole organism levels.
Currently, his lab are studying the following:
• The ionic and metabolic events that lead to cellular dysfunction in the heart and endocrine pancreas.
• The physiology and pathophysiology of human pancreatic islets with respect to incretin biology.
• The design and development of small molecules for the treatment of heart failure, cardiac arrhythmias and type 2 diabetes.
• Ion transport pharmacology.
• ATP-sensitive potassium channel function and molecular pharmacology.
• Anti-diabetic drug pharmacology and cardiovascular safety.
• Molecular optogenetic approaches for the engineering of subcutaneous adipocytes.
• Endogenous light-sensitive signaling pathways in subcutaneous adipocytes.
His research program is currently funded by the Canadian Institutes of Health Research, the Juvenile Diabetes Research Foundation and the Alberta Diabetes Foundation.
Selected Recent Publications
1: Ondrusova K, Fatehi M, Barr A, Czarnecka Z, Long W, Suzuki K, Campbell S,
Philippaert K, Hubert M, Tredget E, Kwan P, Touret N, Wabitsch M, Lee KY, Light PE. Subcutaneous white adipocytes express a light sensitive signaling pathway mediated via a melanopsin/TRPC channel axis. Sci Rep. 2017 Nov 27;7(1):16332.
2: Youssef N, Campbell S, Barr A, Gandhi M, Hunter B, Dolinsky V, Dyck JRB,
Clanachan AS, Light PE. Hearts lacking plasma membrane K(ATP) channels display changes in basal aerobic metabolic substrate preference and AMPK activity. Am J Physiol Heart Circ Physiol. 2017 Sep 1;313(3):H469-H478
3: Fatehi M, Carter CC, Youssef N, Light PE. The mechano-sensitivity of cardiac
ATP-sensitive potassium channels is mediated by intrinsic MgATPase activity. J
Mol Cell Cardiol. 2017 Jul;108:34-41.
4: Fatehi M, Carter CR, Youssef N, Hunter BE, Holt A, Light PE. Molecular
determinants of ATP-sensitive potassium channel MgATPase activity: diabetes risk variants and diazoxide sensitivity. Biosci Rep. 2015 Jul 7;35(4).
5: Baczko I, Leprán I, Kiss L, Muntean DM, Light PE. Future perspectives in the
pharmacological treatment of atrial fibrillation and ventricular arrhythmias in
heart failure. Curr Pharm Des. 2015;21(8):1011-29. Review.
6: Yu Y, Carter CR, Youssef N, Dyck JR, Light PE. Intracellular long-chain acyl
CoAs activate TRPV1 channels. PLoS One. 2014 May 5;9(5):e96597.
7: Soliman D, Wang L, Hamming KS, Yang W, Fatehi M, Carter CC, Clanachan AS, Light PE. Late sodium current inhibition alone with ranolazine is sufficient to
reduce ischemia- and cardiac glycoside-induced calcium overload and contractile
dysfunction mediated by reverse-mode sodium/calcium exchange. J Pharmacol Exp Ther. 2012 Nov;343(2):325-32.
8: Fatehi M, Raja M, Carter C, Soliman D, Holt A, Light PE. The ATP-sensitive
K(+) channel ABCC8 S1369A type 2 diabetes risk variant increases MgATPase
activity. Diabetes. 2012 Jan;61(1):241-9.
9: Lang V, Youssef N, Light PE. The molecular genetics of sulfonylurea receptors
in the pathogenesis and treatment of insulin secretory disorders and type 2
diabetes. Curr Diab Rep. 2011 Dec;11(6):543-51
10: Baczkó I, Husti Z, Lang V, Leprán I, Light PE. Sarcolemmal KATP channel
modulators and cardiac arrhythmias. Curr Med Chem. 2011;18(24):3640-61. Review.
11: Hamming KS, Soliman D, Webster NJ, Searle GJ, Matemisz LC, Liknes DA, Dai XQ, Pulinilkunnil T, Riedel MJ, Dyck JR, Macdonald PE, Light PE. Inhibition of beta-cell sodium-calcium exchange enhances glucose-dependent elevations in
cytoplasmic calcium and insulin secretion. Diabetes. 2010 Jul;59(7):1686-93.