Grant: Master's Award: Canada Graduate Scholarships

For individuals with type 2 diabetes (T2D), glucose-lowering medications are often necessary to regain control over blood glucose (BG) regulation in order to avoid disease-related complications, such as heart and kidney disease, blindness, and nerve damage. Though strict maintenance of BG within a tight range confers the greatest protect against these complications, it is often unattainable due to the risk of hypoglycemia, or low BG. If untreated, symptoms of hypoglycemia can progress from hunger and lightheadedness, to seizure, coma, and even death. Unlike insulin-producing beta cells, these medications incapable of detecting and responding to fluctuations in blood glucose levels, and as a result, they will continually lower BG, even as it approaches and enter the hypoglycemic range. To make matters worse, each exposure to hypoglycemia progressively impair's the body's defences against future episodes, which includes physiological warning signs, like hunger. Patients often raise their BG targets due to fear of hypoglycemia, forcing them to accept a greater risk of long-term complications. This highlights the urgency for better preventative strategies. My laboratory has recently tested a drug, called SSTR2a, that was successful in preventing hypoglycemia in type 1 diabetic rats. It works by blocking the effects of somatostatin, which is a hormone that reduces glucagon activity. As a result, glucagon, the hormone responsible for raising BG levels, was able to maintain stable BG, even in response to an excessive dose of insulin. The goal of my research is to test SSTR2a in rats with T2D. This drug has the potential to change the future of T2D management by relieving the barrier to optimal BG control, while offering more lifestyle freedom and piece of mind.