Our Research Members
Assistant Professor, Department of Psychiatry
Clinician Scientist, Centre for Addiction and Mental Health, Complex Mental Illness
Director of Research, Mental Health and Metabolism Clinic, Centre for Addiction and Mental Health
250 College St.
Toronto, ON M5T 1R8
Phone: 416-535-8501 x4368
Dr. Hahn is a psychiatrist by training, who joined the University of Toronto (U of T) Faculty this spring following completion of a PhD, through the Institute of Medical Sciences, U of T. Her research interests lie in disentangling the complex relationship that underlies the illness of schizophrenia and the 3-5 fold increased risk of type 2 diabetes observed in this population. Her group’s preclinical work has focused on understanding the contribution of antipsychotic medications (which remain the cornerstone of treatment for the illness, but are linked with significant metabolic side-effects) to the risk of glucose dysregulation. Her work to date to elucidate underlying diabetogenic mechanisms of antipsychotics has pointed to specific neurotransmitter systems (i.e. dopaminergic, serotonergic, muscarinic), as well as centrally-mediated mechanisms. As a translational researcher, Dr. Hahn’s work has spanned preclinical rodent and human models of antipsychotic-induced glucose perturbations, including use of complex techniques to measure glucose metabolism (i.e. euglycemic and hyperglycemic clamps, the Frequently Sampled Intravenous Glucose Tolerance Test), and has advanced to studying clinical interventions to mitigate these side-effects.
Associate Professor, Department of Paediatrics, Division of Endocrinology, Director, Centre for Healthy Active Kids
Senior Associate Scientist, Physiology and Experimental Medicine, SickKids Research Institute
My research interests include the clinical and physiologic manifestations of insulin resistance and pancreatic beta cell function in the pediatric age group. I am also interested in treatment studies of childhood obesity. Recent studies include:
(i) risk for diabetes and metabolic syndrome and pathophysiologic mechanisms related to the development of hypothalamic obesity in children treated for craniopharyngioma;
(ii) early life risk factors for the development of obesity and diabetes in infants born to women with gestational diabetes;
(iii) incidence and clinical presentation of type 2 diabetes in Canadian children (iv) role of ectopic fat deposition and metabolic consequences in obese children and adolescents
(v) bariatric surgery outcomes in adolescents
Associate Professor, Department of Nutritional Sciences; Department of Medicine; and Dalla Lana School of Public Health
Canada Research Chair in Diabetes Epidemiology
Associate Scientist, Leadership Sinai Centre for Diabetes, Mount Sinai Hospital
150 College Street
Toronto, ON M5S 3E2
Dr. Hanley’s research interests include the metabolic and nutritional epidemiology of type 2 diabetes and related disorders including obesity, insulin resistance, and beta cell dysfunction, as well as the micro-and macro-vascular complications of type 2 diabetes. His research focuses on diabetes in Aboriginal Canadian communities and other high-risk populations. Current projects include the Sandy Lake Health and Diabetes Project, the PROMISE study, as well as collaborations with the Insulin Resistance Atherosclerosis Study and the Gestational Diabetes and Acute Phase Biomarkers research groups.
Sir John and Lady Eaton Professor and Chair of Medicine
Professor and Clinician Scientist, Division of Rheumatology, Department of Medicine, WCH/Women’s College Research Institute
Professor, Institute for Health Policy, Management and Evaluation, Dalla Lana School of Public Health
Senior Adjunct Scientist, ICES
Toronto, ON M5G 2C4
I am a clinical epidemiologist/health services researcher in the field of osteoarthritis (OA) – I have conducted observational studies examining the relationship between OA and diabetes. Among other findings, we have shown that difficulty walking due to hip or knee OA is an independent risk factor for diabetes complications in people with OA and diabetes, and also a risk factor for incident diabetes.
Associate Professor, Department of Physiology, Faculty of Medicine
Many physiologic processes are mediated by a group of switch-like heterotrimeric G proteins. G proteins are normally coupled to receptors on the cell surface to act as intracellular relays between environmental stimuli and the rest of the cell. Our work defines the biologic importance for precise kinetic regulation of G-protein-mediated signaling events.
Regulation of G-protein signaling pathways: The G-protein heterotrimer is composed of a GDP-bound G alpha subunit and a G beta gamma heterodimer. Upon G-protein activiation, the Galpha subunits are free to engage appropriate downstream effector pathways. Effector signaling is terminated following G alpha catalysed hydrolysis of GTP and reformation of the quiescent receptor-coupled heterotrimer. RGS proteins are a family of GTPase activating proteins (GAPs) for G alpha subunits. By increasing the intrinsic rate of GTP hydrolysis for G alpha subunits, RGS proteins impact GPCR-mediated signaling pathways by: i) promoting faster signal termination kinetics following removal of a physiologic GPCR agonist; and ii) decreasing GPCR agonist sensitivity (i.e. higher agonist concentrations are needed to achieve the same degree of signaling). Our work is aimed at defining the molecular mechanisms that regulate the function of RGS proteins in vivo . Using a combination of physiology, biochemistry, cell biology, pharmacology, and genetics we examine how subcellular localization, G-protein selectivity and interaction with other cellular signaling components regulates the function of RGS proteins in living organisms.
Regulation of G-protein signalling in Pancreatic Islet beta cells: Previous work has shown that one RGS protein family member, RGS4, is highly expressed in beta cells and its function can have profound physiologic effects on insulin secretion. Although the majority of the work in this field has been focussed on the role of RGS4 at the plasma membrane, our recent studies have identified a novel intracellular location for RGS4, the preautophagosome, where it can regulate the autophagic flux and metabolic homeostasis within beta cells. Notably, activated Galphai3 is a potent attenuator of autophagic activity. Accordingly, our work is aimed at understanding the role of RGS4 in the regulation of autophagic flux and enery homeostasis in pancreatic islet beta cells.
Associate Professor, Faculty of Medicine
Head, Divisions of Nephrology and Obstetric Medicine, Sunnybrook Health Sciences Centre
2075 Bayview Ave., Room A206
Toronto, ON M4N 3M5
Phone: 416-480-6100 x3863
Dr. Hladunewich completed her Nephrology Fellowship at Stanford University Medical Center. In addition to her research training in glomerular physiology, she completed a Master’s of Science in Clinical Investigation at Stanford University. Her primary research interest is the long-term sequelae of preeclampsia, including abnormalities in the renin angiotensin system, endothelial dysfunction, insulin resistance and an increased risk for the metabolic syndrome. She also conducts physiologic and outcomes research in young women with pregnancies complicated by diabetic nephropathy. She is a co-investigator in a CIHR-funded study examining the risk of microalbuminuria in women with gestational diabetes.