I. George Fantus, MD, FRCPC
Professor, Department of Medecine, McGill University
Tel.:514-934-1934 ext. 76274
George Fantus graduated from the McGill University Faculty of Medicine followed by postgraduate clinical and research training at McGill, the National Institutes of Health (USA) and the University of Toronto. He was then appointed to McGill and the Royal Victoria Hospital (RVH). He received a Senior Chercheur-Boursier from the FRQS and became Director of the Metabolic Day Centre at the RVH. He was subsequently recruited to the University of Toronto Department of Medicine and to Mount Sinai Hospital and the Lunenfeld-Tanenbaum Research Institute. At the University of Toronto, he served as Director, Division of Endocrinology and Metabolism (2001-2008) and Associate Dean, Research at the Faculty of Medicine (2007-2015). He returned to McGill in 2018. Dr. Fantus received the Young Scientist Award and the Gerald S. Wong Service Award from Diabetes Canada. He is an elected Fellow of the Canadian Academy of Health Sciences.
Insulin resistance, Tyrosine Kinase and phosphatases, glucose metabolism, diabetes complications, oxidative stress.
Research or Clinical Activities
Dr. Fantus’ early research focused on the cellular and molecular mechanism of insulin resistance and the regulation of insulin receptor tyrosine kinase signaling. More recently he has studied glucose toxicity as it relates to both insulin action and the complications of diabetes, in particular diabetic nephropathy. His research has contributed to the understanding of the role of tyrosine phosphatases, oxidative stress and serine/threonine kinases in regulating insulin signaling and the contribution of the hexosamine biosynthesis pathway to the complications of diabetes. Current work is centered on the functional role of the proteins, thioredoxin-interacting protein, and the cellular non-receptor tyrosine kinase, Src, in the pathogenesis of diabetic nephropathy.
Selected Recent Publications
Combined Hyperglycemia- and Hyperinsulinemia-Induced Insulin Resistance in Adipocytes Is Associated with Dual Signaling Defects Mediated by PKC-ζ.
Lu H, Bogdanovic E, Yu Z, Cho C, Liu L, Ho K, Guo J, Yeung LSN, Lehmann R, Hundal HS, Giacca A, Fantus IG. Endocrinology. 2018 Apr 1;159(4):1658-1677. doi: 10.1210/en.2017-00312.
The bradykinin-cGMP-PKG pathway augments insulin sensitivity via upregulation of MAPK phosphatase-5 and inhibition of JNK.
Frigolet ME, Thomas G, Beard K, Lu H, Liu L, Fantus IG. Am J Physiol Endocrinol Metab. 2017 Sep 1;313(3):E321-E334. doi: 10.1152/ajpendo.00298.2016. Epub 2017 Jul 5.
Thioredoxin-Interacting Protein Deficiency Protects against Diabetic Nephropathy.
Shah A, Xia L, Masson EA, Gui C, Momen A, Shikatani EA, Husain M, Quaggin S, John R, Fantus IG. J Am Soc Nephrol. 2015 Dec;26(12):2963-77. doi: 10.1681/ASN.2014050528. Epub 2015 Apr 8.
Inhibition of Src kinase blocks high glucose-induced EGFR transactivation and collagen synthesis in mesangial cells and prevents diabetic nephropathy in mice.
Taniguchi K, Xia L, Goldberg HJ, Lee KW, Shah A, Stavar L, Masson EA, Momen A, Shikatani EA, John R, Husain M, Fantus IG. Diabetes. 2013 Nov;62(11):3874-86. doi: 10.2337/db12-1010. Epub 2013 Aug 13
Thioredoxin-interacting protein mediates high glucose-induced reactive oxygen species generation by mitochondria and the NADPH oxidase, Nox4, in mesangial cells.
Shah A, Xia L, Goldberg H, Lee KW, Quaggin SE, Fantus IG. J Biol Chem. 2013 Mar 8;288(10):6835-48. doi: 10.1074/jbc.M112.419101. Epub 2013 Jan 17.