Role of Amyloid in Failure of Transplanted Human Islets

In Type 1 diabetes, beta cells are destroyed by the immune system, leaving the body unable to produce insulin. Type 1 diabetic patients inject insulin several times a day to normalize their blood glucose levels. Estimating the correct dose of insulin to administer is difficult: too much insulin leads to hypoglycemic shock, while chronic hyperglycemia (a shortage of insulin) can lead to organ damage and related complications such as blindness, kidney failure, neuropathies, vascular damage and pain in the limbs. The transplantation into diabetics of insulin-producing islet cells shows promise for relief from daily insulin injections and the development of diabetic complications. However, islet transplantation is in the early stages, and long-term rates of transplanted islet graft survival and maintained function are low: only 10 per cent of islet transplanted recipients remained free from insulin injections five years post-transplantation. Kathryn Potter is working to better understand the mechanisms underlying graft failure. In particular, she is interested in how stressors unrelated to immunity—such as pre-transplant and post-transplant hyperglycemia and the use of immunosuppressants—may cause dysfunction in transplanted beta cells and lead to graft failure. Her research may lead to modifications to current transplantation protocols that improve long-term islet transplantation success rates.