Profiles of BBDC Members Primarily Involved In Diabetes Research

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Retnakaran, Ravi - MD, FRCPC

University of Toronto Appointment(s): Associate Professor, Department of Medicine, Division of Endocrinology and Metabolism

Other Appointment(s):  
 
 

Contact Information:
60 Murray Street, Suite L5-025, Mailbox 21
Toronto, ON   M5T3L9

Phone: 416-586-4800 ext 3941
Fax: 416-586-8853
Email: rretnakaran@mtsinai.on.ca

Diabetes Related Research Activities:

My research focuses on the early pathophysiology of type 2 diabetes (T2DM) and cardiovascular disease (CVD). A central component of this program is a large prospective observational cohort study of women recruited in pregnancy and followed longitudinally for several years postpartum. The concept underlying this program is that the gluco-regulatory response to the metabolic challenge posed by pregnancy provides unique physiologic insight into a woman's future risk of metabolic and vascular disease. Indeed, in a series of papers, we have demonstrated that a woman's glucose tolerance status in pregnancy provides a window to her future risk of both T2DM and CVD, ranging from high risk (in women with gestational diabetes (GDM)) to intermediate risk (in women with mild abnormalities of glucose tolerance in pregnancy) to low risk (in women that maintain normal antepartum glucose homeostasis). Thus, longitudinal cardio-metabolic characterization of a cohort of women reflecting the full spectrum of glucose tolerance in pregnancy can provide insight into early events in the pathophysiology of T2DM and CVD. The other main element of our research program is a series of clinical trials aimed at preservation of pancreatic beta-cell function early in the course of T2DM.

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Rocheleau, Jonathan V. - PhD

University of Toronto Appointment(s): Associate Professor, Institute of Biomaterials and Biomedical Engineering; Department of Medicine; Department of Physiology

Other Appointment(s): Affiliated Scientist, Toronto General Research Institute, University Health Network

Contact Information:

MaRS Centre, Toronto Medical Discovery Tower
101 College Street
10th Floor, Room 10-707
Toronto , Ontario M5G 1L7

Phone: 416-581-7839
Fax: 416-581-7839
Email: jon.rocheleau@utoronto.ca
Websites: http://quantm3.weebly.com

Diabetes Related Research Activities:

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.

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Rogers, Ian - PhD

University of Toronto Appointment(s): Primary appointment: Assistant Professor, Department of Obstetrics and Gynecology
Cross Appointment: Department of Physiology

Other Appointment(s): Women's and Infants Health, Obs/Gyn, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto

Contact Information:
Toronto Center For Phenogenomics, Room 5-1015
25 Orde St.
Toronto, ON   M5T 3H7

Phone: 416-586-4800
Email: rogers@lunenfeld.ca

Diabetes Related Research Activities:

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.

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Rosella, Laura - PhD, MHSc

University of Toronto Appointment(s): Assistant Professor, Dalla Lana School of Public Health

Other Appointment(s): Scientist, Public Health Ontario | Santé publique Ontario
Adjunct Scientist, Institute for Clinical Evaluative Sciences (ICES)

Contact Information:
Suite 300
480 University Ave.
Toronto, ON   M5G 1V2

Phone: (647) 260-7416
Fax: (647) 260-7600
Email: laura.rosella@oahpp.ca
Websites: http://www.dlsph.utoronto.ca/faculty-profile/laura-c-rosella

Diabetes Related Research Activities:

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) (Rosella et. al, JECH, 2011), which is the only existing only tool built to inform population intervention strategies for diabetes (BMJ 2011). This work is recognized as a novel way to inform to diabetes preventions strategies and is currently being used by policymakers in Canada. We are currently working on methods to estimate the future health care and cost burden associated with type 2 diabetes in Canada and developing and validating improved tools that will allow decision-makers to better target and design population interventions in several regions across Canada. In addition, I am currently leading an investigation studying various approaches to improve screening for type 2 diabetes in the population.

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Rozakis Adcock, Maria

University of Toronto Appointment(s): Associate Professor, Department of Laboratory Medicine & Pathobiology

Other Appointment(s):  
 
 

Contact Information:

University of Toronto, Medical Sciences Building
1 King's College Circle, Room 6238
Toronto, Ontario M5S 1A8

Phone: 416-946-0392
Fax: 416-978-5959
Email: maria.rozakis@utoronto.ca

Diabetes Related Research Activities:

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 β-cell destruction that outweighs the rate of β-cell replication and renewal. Currently, the factors that instigate an increased rate of β-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.

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