Profiles of BBDC Members Primarily Involved In Diabetes Research

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Mahadevan, Radhakrishnan - Ph.D.

University of Toronto Appointment(s): Associate Professor, Chemical Engineering and Applied Chemistry, Institute of Biomaterials and Biomedical Engineering

Contact Information:
Wallberg Building 326
200 College Street
Toronto, ON   M5S 3E5

Phone: (416) 946-0996
Fax: (416) 978-8605

Diabetes Related Research Activities:

We aim to use a systems biology approach for understanding the mechanisms behind and diabetes and the role of potential therapeutic strategies. Our focus is on describing glucose, insulin, glucagon, TAG, levels at the whole body level using an multi-scale metabolic model.  We hope to integrate phenomena across spatial scales from cellular to tissue to organ as well as temporal scales from s-min to hours.  Using these models, we aim to understand the sensitivity of the different factors affecting this complex disease.

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Mahmud, Farid H. - MD, FRCPC

University of Toronto Appointment(s): Assistant Professor, Faculty of Medicine

Other Appointment(s): Division of Pediatric Endocrinology, The Hospital for Sick Children

Contact Information:

The Hospital for Sick Children
555 University Avenue
Toronto, Ontario M5G 1X8

Phone: 416-813-6218
Fax: 416-813-6304

Diabetes Related Research Activities:

As a pediatric endocrinologist who cares for children with diabetes, obesity and other chronic medical conditions on a daily basis, I am concerned about the prospects for their future health. This has driven me to seek answers to some of the meaningful questions that are going to benefit their health and this has prompted me to pursue a clinical research program. My research interests include the study of conditions associated with type 1 diabetes, such as celiac disease and the evaluation of early atherosclerotic risk factors in young patients with endocrine conditions who are at high risk of cardiovascular disease including both type 1 and type 2 diabetes, insulin resistance and obesity. I have conducted clinical studies to identify patients at risk and study the impact of this process on the health of these children.

These studies are also evaluating interrelated risk factors for atherosclerosis in these high risk populations and the effectiveness of lifestyle, diet and drug therapy treatment strategies.  Specifically we evaluated dietary intake in patients with type 1 diabetes as well as standardized activity assessments which showed high rates of dietary fat intake and inactivity, which worsened during adolescence. As part of my research, I adapted an innovative method to study endothelial function as a marker of early atherosclerosis which we able to evaluate as a reversible indicator of disease with the potential to assess the effectiveness of different treatment strategies on reducing early atherosclerotic changes. 

Longer term, the findings of this research will be used to develop guidelines for clinical practice, prevention and treatment strategies. It is hoped that the effective translation of this research into clinical practice will help to manage cardiovascular disease risk in children with the ultimate goal of cardiovascular disease prevention.

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Mamdani, Muhammad - PharmD, MA, MPH

University of Toronto Appointment(s): Professor, Institute of Health Policy, Management, and Evaluation of the Faculty of Medicine and the Leslie Dan Faculty of Pharmacy

Other Appointment(s): Director, Applied Health Research Centre, Li Ka Shing Knowledge Institute,St. Michael's Hospital

Contact Information:
Li Ka Shing Knowledge Institute
30 Bond Street

Phone: 416-864-3037
Fax: 416-864-3014

Diabetes Related Research Activities:

The Applied Health Research Centre (AHRC) is a comprehensive, not-for-profit, academic clinical research centre that houses leading clinical research methodologists and statisticians as well as operations experts including contracts and finance experts, study management coordinators, and research informatics specialists. Further, the AHRC also houses industry-standard and highly secure data management infrastructure. The AHRC has extensive experience designing and implementing phase 2b-4 clinical trials as well as nonrandomized studies such as patient registries and retrospective database studies. The infrastructure and support services are available to all academic clinical researchers and is well suited for diabetes-related clinical research.

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McCulloch, Christopher - PhD, DDS, Certificate in Periodontics

University of Toronto Appointment(s):

  • Professor, University of Toronto, Faculty of Dentistry
  • Cross-appointed to Department of Laboratory Medicine and Pathobiology, Faculty of Medicine

Other Appointment(s):

  • Canada Research Chair in Matrix Dynamics
  • Director, Matrix Dynamics Group, Faculty of Dentistry
  • Full Member, School of Graduate Studies
  • Director, CIHR STIHR, “Cell Signalling in Mucosal Health and Disease"
  • Consultant, Royal College of Dental Surgeons of Ontario (RCDSO), Toronto, ON

Contact Information:
FitzGerald Building, Room 244
150 College Street
Toronto, ON   M5S 3E2

Phone: 416-978-1258
Fax: 416-978-5956

Diabetes Related Research Activities:

My laboratory is focused on the signals arising from the extracellular matrix that regulate the metabolic activities of fibroblasts. In the context of diabetes, I am interested in the notion that diabetes-induced glycation of collagen may impact the function and differentiation of fibroblasts in the cardiac interstitium. Accordingly, I cardiac fibroblasts may convert to myofibroblasts, cells that contribute to the fibrosis that is observed in diabetic cardiomyopathy.

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McGaha, Tracy - PhD, MS, BS

University of Toronto Appointment(s): Associate Professor, Department of Immunology

Other Appointment(s): Senior Scientist, Princess Margaret Cancer Centre, Tumor Immunotherapy Program

Contact Information:
Princess Margaret Cancer Centre
610 University Ave., Room 8-410
Toronto, ON   M5G 2M9

Phone: (416) 634-7252

Diabetes Related Research Activities:

We are interested in the  endoplasmic reticulum stress/unfolded protein response (UPR) and integrated stress response (ISR) signals as drivers of macrophage (MF) phenotype and tissue destruction in autoimmune diabetes (T1D).

MF infiltration in the islets is a well-established mechanistic driver of insulitis and b cell death in T1D. Functionally, infiltrating MF in pancreatic lesions exhibit an inflammatory phenotype with NADPH-driven superoxide and ROS production and TNF-a and IL-1b secretion (in a STAT1-dependent mechanism). Via production of these effector molecules, MF act in a synergistic fashion with infiltrating dendritic cells and T cells to drive islet cell dysfunction and death. Conversely, modulating MF phenotype has a dominant impact on the course of disease in experimental models of spontaneous and induced T1D, reducing the onset and severity of insulitis. Given this, manipulation of MF function becomes an attractive therapeutic target in T1D to control autoimmune pathology and as a tool to promote transplant tolerance.

Cellular stress signals play a key role in myeloid inflammatory potential. UPR stress can drive JNK and STAT1 activation, promote TNFa secretion, and inflammasome maturation/IL-1b production in MF and DC. Likewise the ISR plays a dominant role in controlling MF phenotype and inflammatory potential. For example, our lab demonstrated the ISR kinase GCN2 regulates IL-6 and IL-12 production promoting endotoxemic mortality. However, stress signals can also suppress inflammation as reactive oxygen species driven ER stress promotes myeloid-dependent immune suppression in tumors. Further, we have found GCN2 suppresses inflammatory T cell proliferation and systemic autoimmunity.   Importantly modification of stress signaling by pharmacologic approaches has a potent impact on outcomes in inflammation, transplantation, autoimmunity and cancer. These striking findings show stress signaling is a cell and context-dependent modifier of immune function providing novel druggable targets; however, it is paramount to clearly delineate the role (either pro- or anti-inflammatory) of stress signaling modules in the pathologic process.

In our research project we are examining the role of metabolism and stress signaling in inflammatory pathology in T1D using mouse models of disease. Moreover we are examining the follow-on prediction that manipulation of MF phenotype via antagonists or agonists of UPR stress and/or the ISR will modulate the phenotype of MF; thereby reducing autoimmune pathophysiology and/or promoting islet transplant acceptance. 

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