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Search for new treatments - Currently Funded

Dr. Patricia L. Brubaker (Operating Grant funded 2010-2013)

University of Toronto (Toronto, ON)

Title: Mechanisms underlying secretion of the insulinotrophic hormone, glucagon-like peptide-1

After meals, intestines release a small protein called GLP-1. This protein causes the pancreas to secrete more insulin to regulate blood sugar. Synthetic GLP-1 is currently used to treat diabetes, so Dr. Patricia L. Brubaker is trying to find ways to boost the body's natural GLP-1 in hopes of finding new ways to treat type 2 diabetes.

 

Dr. Jean Buteau (Scholar Award funded 2008-2013)

Universite Laval (Québec, QC)

Title: Glucagon-like peptide-1 and beta cell neogenesis

Dr. Jean Buteau is studying whether the hormone GLP-1 promotes the growth of new insulin-secreting beta cells and how this happens. Dr. Buteau's research is helping to find new ways to help the body grow new beta cells as a possible treatment for both type 1 and 2 diabetes.

 

Dr. Claudia Gagnon (Operating Grant funded 2012-2015)

Universite Laval -CRCHUL (Québec, QC)

Title: Role of vitamin D in the prevention and treatment of diseases associated with insulin resistance.

Low levels of vitamin D are associated with an increased risk of developing insulin resistance, a risk factor for developing type 2 diabetes. Dr. Claudia Gagnon will study people with insulin resistance for six months. Half of the people will take vitamin D supplements, and half will take a placebo (a pill that contains no vitamins or drugs, often called a "sugar pill"). Dr. Gagnon's team will then study whether vitamin D improves insulin resistance, cholesterol levels, blood pressure, or body weight. This research project will determine if taking vitamin D supplements, a cheap and safe strategy, could prevent or treat diseases associated with insulin resistance.

 

Dr. Carol T. L. Huang (Operating Grant funded 2012-2015)

University of Calgary (Calgary, AB)

Title: Placenta hormones as adjunct in treatment of diabetes

In diabetes, the body either does not make enough insulin (the hormone that lowers blood glucose), or does not properly use the insulin that is made, leading to high blood glucose. Diabetes could be treated or reversed if the body could make enough insulin‐producing cells (called beta cells) to meet their insulin requirements. Dr. Carol Huang and her team found that the pregnancy hormone, prolactin, helps keep normal blood sugars in pregnant mice by causing beta cells to divide. The result is a higher number of beta cells which produce more insulin. Based on this discovery, Dr. Huang's laboratory team will test if prolactin or related hormones could be used to treat or reverse type 1 and type 2 diabetes.

 

Dr. Tianru Jin (Operating Grant funded 2010-2013)

University Health Network (Toronto, ON)

Title: Re-assess mechanisms underlying the function of the incretine hormone glucagon-like-peptide-1 and Exendin-4

Dr. Tianru Jin is examining a hormone called glucagon-like peptide 1 (GLP-1). This hormone increases the production and release of insulin, protects the beta cells (insulin-producing cells) of the pancreas, and tells the beta cells to multiply. Some new drugs to treat type 2 diabetes attempt to mimic the actions of GLP-1, but they are not first-choice treatments. Dr. Jin is investigating how GLP-1 acts in hopes of finding ways to create new drugs to treat both type 1 and type 2 diabetes.

 

Dr. Min Suk Kim (Postdoctoral Fellowship Award funded 2010-2013)

Samuel Lunenfeld Res. Inst./Mount Sinai Hospital (Toronto, ON)

Supervisor: Dr. Daniel J. Drucker

Title: The role of incretins and dipeptidyl peptidase-4 in the pathophysiology of atherosclerosis

Two recently approved drug types for the treatment of type 2 diabetes are called GLP-1 receptor agonists (exenatide, liraglutide) and DPP-4 inhibitors (sitagliptin, vildagliptin, saxagliptin). Dr. Min Suk Kim is investigating what effect these therapies have on the development of atherosclerosis (narrowed blood vessels) using a mouse model of diabetes. The results of our studies may provide important new information about the safety and efficacy of new anti-diabetes medications, with a specific focus on whether these drugs can reduce the development of atherosclerosis.

 

Dr. Peter E. Light (Operating Grant funded 2010-2013)

University of Alberta (Edmonton, AB)

Title: Endocrine cell sodium/calcium exchange and glucose homeostasis

Current medications for type 2 diabetes include drugs that stimulate the production of insulin. These drugs act no matter if blood sugar is high or low, so they can cause times of dangerously low blood sugar. Dr. Peter E. Light is examining a specific part of the pancreatic beta cells to determine if there is a way to create a drug that stimulates the production of insulin only when blood sugar is high, thus avoiding both dangerously low and dangerously high blood sugar.

 

Dr. Jun-Li Liu (Operating Grant funded 2011-2014)

McGill University Health Centre (Montréal, QC)

Title: The anti-diabetic effects of Reg proteins induced by duodenal-jejunal bypass in obese rodents

Dr. Liu is investigating the anti-diabetic effects of bariatric surgery in rats and whether or not part of that effect is due to an increased expression of Reg proteins in the intestine and/or pancreas, which promote beta cell expansion and insulin secretion. This research could help shed light on the benefits induced by bariatric surgery and improve treatment for type 2 diabetes.

 

Dr. Jonathan Z. Long (Postdoctoral Fellowship Award funded 2012-2015)

Dana-Farber Cancer Institute (Boston, MA, United States of America)

Supervisor: Dr. Bruce M. Spiegelman

Title: Enzymatic regulation of PPARgamma ligands

People with type 2 diabetes are sometimes prescribed a drug called rosiglitazone. This drug works by "turning on" a molecule called PPARgamma, which regulates fat tissues. Dr. Jonathan Long aims to identify if there are other molecules that turn PPARgamma on that exist naturally in our bodies. Dr. Long is specifically searching for enzymes that regulate PPARgamma, and will investigate candidates to determine how they regulate PPARgamma in the body. Dr. Long hopes that understanding these mechanisms will allow for the future development of new diabetes drugs.

 

Dr. Arturo Mancini (Postdoctoral Fellowship Award funded 2012-2015)

University of Montréal (Montréal, QC)

Supervisor: Dr. Vincent Poitout

Title: Novel G-protein coupled receptors implicated in pancreatic beta-cell function and viability.

Beta cells in the pancreas produce insulin, the hormone that lowers blood glucose. In type 2 diabetes, normal beta cell function and number is lost, which leads to high blood glucose levels. Ideally, interrupting this process could delay or even prevent type 2 diabetes and diabetes-related complications. Dr. Arturo Mancini is investigating a family of molecules – called GPCRs – that regulate beta cell insulin release. Dr. Mancini is specifically looking at two GPCRs whose function is unknown. He will identify if and how these molecules control insulin production and release in beta cells and if they allow beta cells to survive longer.

 

Dr. Joanne E. McBane (Postdoctoral Fellowship Award funded 2012-2014)

University of Ottawa Heart Institute (Ottawa, ON)

Supervisor: Dr. Erik J. Suuronen

Title: Evaluating collagen-based matrices to pre-vascularize an ectopic islet transplant site

People with type 1 diabetes cannot produce insulin, the glucose lowering hormone, and need to monitor blood glucose levels and must be treated with insulin. One possible treatment for type 1 diabetes is transplanted islet cells (the cells that produce insulin). Islet transplants do not always function in the long term, partly because they don't get enough blood and oxygen to remain healthy. Dr. Joanne McBane hopes to use a natural protein (collagen) to increase blood flow to islet transplants. If successful, the collagen implant developed from this project could allow more people with type 1 diabetes to remain insulin independent after islet transplantation.

 

Dr. Erin E. Mulvihill (Postdoctoral Fellowship Award funded 2011-2014)

Mount Sinai Hospital (Toronto, ON)

Supervisor: Dr. Daniel J. Drucker

Title: Incretin control of intestinal lipid metabolism

Patients with type 2 diabetes develop increased lipid production from both the intestine and liver, resulting in increased circulating levels of fatty particles in the blood. Increased concentrations of lipids (cholesterol and triglyceride) can damage tissues, particularly once deposited in the walls of the arteries, contributing to an increased risk of cardiovascular disease in people with diabetes. New therapies based on GLP-1 ( glucagon-like peptide-1) action have recently been approved for the treatment of type 2 diabetes. Dr. Mulvihill is investigating how these drugs influence the production of intestinal lipoproteins, and whether the actions of these agents can influence cardiovascular risk. This research could help find new ways to prevent the over-production and export of lipids from intestinal cells and to decrease the risk of type 2 diabetes and atherosclerosis.

 

Dr. Rémi Rabasa-Lhoret (Operating Grant funded 2012-2014)

Clinical Research Institute of Montréal (IRCM) (Montréal, QC)

Title: Closed-loop control of glucose levels in type 1 diabetes: preliminary clinical trials

Normally, blood glucose levels are controlled by two hormones: insulin lowers blood glucose; and glucagon raises blood glucose. People with type 1 diabetes must receive insulin by injection or by a continuous insulin infusion pump (CSII), but many can still face large swings from high to low blood glucose, which can lead to long‐term health complications and reduce quality of life. Dr. Rémi Rabasa‐ Lhoret and his team have created a closed‐loop system (CLS) (or "wearable artificial pancreas"), including a continuous glucose sensor to read blood glucose changes, an infusion pump to provide insulin (single‐hormone CLS) or insulin and glucagon (dual‐hormone CLS), and a computer program that uses information from the sensor to tell the pump how much of each hormone to give. Dr. Rabasa‐ Lhoret and his team will compare the dual‐hormone CLS, the single‐hormone CLS, and the traditional CSII over a controlled period of 24 hours to determine the benefits of each system. The CLS has a great potential to improve people's quality of life, health outcomes, promote physical activities, and lift the burden of diabetes management from the patients and their health care providers.

 

Dr. Maria Rozakis Adcock (Operating Grant funded 2010-2013)

University of Toronto (Toronto, ON)

Title: Novel genetic animal models of PHIP1

Dr. Maria Rozakis Adcock is examining why insulin-producing cells lose their function in type 2 diabetes. She has found a molecule that is able to reverse high blood sugar in obese diabetic animals. Dr. Rozakis Adcock is further testing this molecule in order to understand its role in regenerating insulin-producing cells damaged in diabetic states. Her research could lead to new ways to prevent or treat type 2 diabetes.

 

Dr. Pere Santamaria (Operating Grant funded 2010-2013)

University of Calgary (Calgary, AB)

Title: The contribution of 'bystander' autoreactive T-cell memory to islet allograft failure in spontaneously diabetic hosts

In type 1 diabetes, the immune system attacks insulin-producing cells (islet cells). Dr. Pere Santamaria is looking at how the immune system recognizes islet cells, in hopes of finding a way to increase the success of transplanting healthy islet cells in people with type 1 diabetes.

 

Dr. C. Bruce Verchere (Operating Grant funded 2011-2014)

University of British Columbia (Vancouver, BC)

Title: Islet Amyloid and Islet Transplant Failure

Replacement of insulin-producing beta cells by islet transplantation is a promising approach for the treatment of type 1 diabetes, but is still limited by the low number of available donors and loss of beta cells during islet isolation, culture and following transplantation. Dr. Verchere has found that islet amyloid, a toxic lesion of the pancreatic islets previously thought to be present only in type 2 diabetes, forms rapidly in transplanted human islets and may be an important cause of beta cell death, contributing to graft failure. He is trying to determine whether inhibition of amyloid formation in transplanted human islets will protect beta cells from the toxic effects of rapid amyloid formation and enhance the survival and function of human islet transplants. This research may lead to a new way to enhance survival and function in transplanted human islets, and may improve success of clinical islet transplantation in people with type 1 diabetes.

 

Previously Funded