Grant: Doctoral: Vanier Canada Graduate Scholarships

Type 1 diabetes is a condition where the body's own immune system attacks the cells in the pancreas that make the hormone insulin. When the insulin producing cells (called beta-cells) are destroyed, the resulting high blood sugar leads to a number of secondary diseases. We know that the immune system is involved, but we still do not know how or why the insulin producing cells are killed. So far, all efforts to treat type 1 diabetes involves 'turning down' the immune system and no available drugs protect the beta-cells directly. The Johnson lab has developed automated ways of searching for drugs that protect beta-cells from death when they are exposed to type 1 diabetes-like conditions. We have found that a drug called carbamazepine, FDA approved for epilepsy, is effective at blocking beta-cell death. Encouragingly, our lab has confirmed that carbamazepine dramatically reduces type 1 diabetes in mice. Carbamazepine works by blocking channels that let sodium into the cell and beta-cells have lots of a certain type of sodium channel that neighbouring cells do not have as much of. The goal of my graduate project will be to understand exactly how this drug protects mice from diabetes and to develop, along with our collaborators, even more effective versions of this drug. Finally, we want to figure out whether blocking the sodium channel specific to the beta cell is enough to prevent type 1 diabetes. These studies are important because it will test whether sodium channels are a good target for type 1 diabetes therapy, and whether existing drugs can be re-purposed to treat type 1 diabetes. If the results of this study confirm our current hypothesis, we may have a new way of treating of treating type 1 diabetes that is specific to beta cells and does not block the immune system, limiting side effects and avoiding concerns like secondary infections and cancer. Our ultimate goal is to find effective ways to protect insulin producing beta-cells from death in type 1 diabetes.