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Dr. George Fantus
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Dr. George Fantus
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Dr. Fantus is currently an Associate Scientist at the Samuel Lunenfeld Research Institute of Mount Sinai Hospital, as well as a senior scientist at the Toronto General Hospital Research Institute and Director of the Core Laboratory of the Banting and Best Diabetes Centre at the University of Toronto. His clinical work in endocrinology and on Type 2 diabetes is located at the Mount Sinai Hospital/University Health Network, Division of Endocrinology and Metabolism. 

In his lab, Dr. Fantus uses cultured cells and mouse models to investigate the molecular mechanism of insulin resistance and the “toxic” effects of high glucose that accompany diabetes. He is looking into the role of various kinases, phosphatases and signaling pathways that are responsible for sensitizing cells to the effects of insulin.

 
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Jul 05, 2011 12:00 AM

     

At a Glance

  • Dr. Fantus’ lab aims to determine the mechanisms behind insulin resistance toward new treatments and methods to prevent insulin resistance.

  • His research interests include the mechanism of insulin signal transduction, with a specific focus on insulin resistance and Type 2 diabetes.

  • Dr. Fantus also investigates various molecular complications involved in diabetes, specifically diabetic nephropathy.

  • In 1993, he received the Young Scientist Award from the Canadian Diabetes Association, and he has published over 100 articles.

  


Major Research Activities

Dr. Fantus has discovered ways by which abnormal glucose metabolism due to hyperglycemia can alter gene expression. Studies are carried out in insulin-resistant target tissues, adipocytes and muscle cells to determine changes in enzyme activation, protein-protein interactions and glucose transport.

Dr. Fantus’ lab also undertakes investigations to define the pathogenesis of diabetic nephropathy. His work on this includes studying the effects of high glucose on cell signaling, oxidative stress, excess O-glycosylation and abnormal gene expression.

 

Recent Publications

Masson, E., Koren, S., Razik, F., Goldberg, H., Kwan, E.P., Sheu, L., Gaisano, H.Y., Fantus, I.G. Thioredoxin-interacting protein-deficient mice are resistant to streptozotocin-induced diabetes but exhibit a defect in insulin secretion. Am. J. Physiol. Endo. Metab. 206:E1251-E1261, 2009.

Sun J, Khalid S, Rozakis-Adcock M, Fantus IG, Jin T. P-21 activated protein kinase-1 functions as a linker between insulin and Wnt signaling pathways in the intestine. Oncogene 28: 3132-3144, 2009.

Whiteside, C., Wang, H., Xia, L., Munk, S., Goldberg, H.J., Fantus, I.G. Rosiglitazone prevents high glucose-induced vascular endothelial growth factor and collagen IV expression in cultured mesangial cells. Exp. Diabetes Res. 2009:910783, 2009.

Khalid S, Hwang D, Babichev Y, Kolli R, Altamentova S, Koren S, Goodwin PJ, Ennis M, Pollak M, Sonenberg N, Fantus IG. Evidence for a tumor promoting effect of high fat diet independent of insulin resistance in HER2/Neu mammary carcinogenesis. Breast Can Res Treat 122:647-659, 2010

Sison, K., Eremina, V., Baelde, H., Hiroshima, M., Rossant, J., Fantus, I. G., Quaggin, SE. Glomerular structure and function require paracrine, not autocrine, VEGF-VEGRF-2 signaling. J. Am Soc. Nephrol. 21:1691-1701, 2010

Shao W, Yu Z, Fantus IG, Jin T. Cyclic AMP signaling stimulates proteasome degradation of thioredoxin interacting protein (TxNIP) in pancreatic beta-cells. Cell Signaling, 8:1240-1246, 2010.

Li L, Hossain MA, Sadat S, Hager L, Liu L, Tam L, Schroer S, Huogen L, Fantus IG, Connelly PW, Woo M, Ng DS. Lecithin cholesterol acyltransferase null mice are protected from diet-induced obesity and insulin resistance in a gender-specific manner through multiple pathways. J. Biol. Chem. 286(20): 17809-17820, 2011.

Liang SB, Yang XZ, Trieu Y, Li ZH, Zive J, Leung-Hagesteijn C, Wei E, Zozulya S, Coss CC, Dalton JT, Fantus IG, Trudel S. Molecular target characterization and anti-myeloma activity of the novel, insulin-like growth factor 1 receptor inhibitor, GTx-134. Clin Cancer Res 2011 Jun 1 [Epub ahead of print].

Goldberg H, Whiteside C, Fantus IG. Basal O-linked b-N-acetylglucosamine (O-GlcNAc) supports p38 MAPK activation by high glucose in glomerular mesangial cells. Am J Physiol. (In press) 2011.

 

 

 

► Lunenfeld Research Repository

 

 

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