Our Research Members
Professor, Department of Medicine, Division of Endocrinology and Metabolism
60 Murray Street, Suite L5-025, Mailbox 21
Toronto, ON M5T 3L9
Phone: 416-586-4800 x3941
My research program focuses on the pathophysiology and treatment of type 2 diabetes (T2DM), with a particular interest in the potential reversibility of pancreatic beta-cell dysfunction early in the course of diabetes. In this context, our research group is conducting a series of innovative clinical trials evaluating novel therapeutic strategies for the preservation of beta-cell function in early T2DM, including the CIHR-funded RESET IT Trial and PREVAIL Trial. In addition, our research program has highlighted the concept that a women’s gluco-regulatory response to the metabolic challenge posed by pregnancy can provide unique insight into her future risk of T2DM and cardiovascular disease later in life. This concept is being studied with CIHR-funded prospective observational cohorts in Toronto and China.
Percy Edward Hart and Erwin Edward Hart Professor in Biomedical Engineering
Associate Director Research
Institute of Biomaterials and Biomedical Engineering, Faculty of Applied Science and Engineering
Scientist, Toronto General Research Institute, University Health Network
Interaction between pancreatic islets and vascular endothelial cells is necessary for the maintenance of beta-cell mass and function. Aside from acting as a conduit for molecular oxygen, vascular endothelial cells in vivo secrete the majority of islet extracellular matrix (ECM). This ECM likely provides a permissive signal for beta-cell proliferation, contributing to the coordinated hyperplasia of these tissues during the early stages of Type 2 diabetes. This ECM also provides a reservoir for heparin binding growth factors that further modulate this hyperplasia, including fibroblast growth factor (FGF) and vascular endothelial growth factor-A (VEGF-A). We hypothesize that communication between beta-cells and vascular endothelial cells directs the proliferation and function of both tissues.
Primary appointment: Assistant Professor, Department of Obstetrics and Gynecology
Cross Appointment: Department of Physiology
Women’s and Infants Health, Obs/Gyn, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto
25 Orde St.
Toronto, ON M5T 3H7
My lab uses progenitor cells and human pluripotent stem cells as a basis for developing cell based therapies for the treatment of Diabetic symptoms. We are investigating the wound healing properties of blood cells and mesenchymal cells in a model of Peripheral Vascular Disease (PVD) and Diabetic skin wounds. My lab has demonstrated that blood cells have strong paracrine signaling that can reduce inflammation and apoptosis while promoting angiogenesis. Together, this results in superior tissue repair. We have demonstrated this in a spinal cord injury model, a hind limb ischemia model and a diabetic wound healing model. We have concluded that blood cells improve the neurological function of spinal cord injured rats by paracrine signaling that have a positive effect on tissue repair through a decrease in inflammation and an increase in angiogenesis. A siimilar mechanism accounts for improved tissue repair in the PVD model and the diabetic wound healing model (using db/db mice). The results obtained in all three models demonstrate that there is a common mechanism of tissue repair and the same preparation of cells can work in multiple clinical situations. We are currently working with the Center for the Commercialization of Regenerative Medicine (CCRM) with a grant from the Stem Cell Network, to develop the diabetic wound healing project. CCRM is working with us on the large scale manufacturing of the cells and with the development of biomaterials as a cell carrier.
We are also collaborating with the Nagy lab on the regeneration of islets using reprogrammming methods developed for pluripotent cells. My lab is developing an in vitro model of islet development using iPS cells to better understand islet physiology. This model will then be used in collaboration with the Nagy lab to investigate the feasibility of reprogramming different cell types to directly aid in the regeneration of islets damaged in type 1 diabetic patients.
Assistant Professor, Dalla Lana School of Public Health
Scientist, Public Health Ontario | Santépublique Ontario
Adjunct Scientist, Institute for Clinical Evaluative Sciences (ICES)
The goal of my research is to inform the prevention of type 2 diabetes in the population. My research is focused on the use of advanced epidemiologic & biostatical approaches on large population-based data to inform public health activities targeted at reducing type 2 diabetes and obesity. I specialize on the development of population risk tools and have led methodological advances in the new field of risk algorithms applied to the population setting. I recently led the development of the Diabetes Population Risk Tool (DPoRT), which is the only existing only tool built to inform population intervention strategies for diabetes. This work is recognized as a novel way to inform to diabetes preventions strategies and is currently being used by policymakers in Canada. I have also led the largest study estimating diabetes-attributale health care costs as well as the burden of undiagnosed diabetes in Canada.
Associate Professor, Department of Laboratory Medicine & Pathobiology
1 King's College Circle
Toronto, ON M5S 1A8
The prevalence of obesity is increasing worldwide, as is the prevalence of obesity-related co-morbidity. Obesity is associated with an increased risk of developing insulin resistance and Type II diabetes (T2D). A universal observation in both humans and rodents is that impaired insulin secretion in is caused by a marked increase in pancreatic B-cell destruction that outweighs the rate of B-cell replication and renewal. Currently, the factors that instigate an increased rate of B-cell death during the pathogenesis of T2D are not fully understood. Research in the Rozakis lab is focused on understanding molecular and cellular processes that contribute to insulin resistance and Type II diabetes. Our lab has identified novel transcriptional networks that serve to regulate pancreatic islet regeneration and glucose homeostasis. We use a combination of biochemical, proteomic approaches and transgenic animal models to understand the molecular circuitry involved in transducing the unique actions of insulin on its target tissues.