Type 1 diabetes (T1D) involves reduced function and loss of the insulin-producing beta cells of the pancreas. Current treatment of T1D patients for increased blood glucose levels involves insulin injection. However, the level of insulin injected often does not match the blood glucose level. This frequently results in a decrease in blood glucose level below its normal levels (hypoglycemic episodes). This event is a significant health risk in T1D.

Studies showed that beta cells become less efficient in releasing insulin at very early stages of T1D. During these stages, even a moderate level of insulin release from beta cells results in reduced rates of T1D-related problems. Hence, there is great interest in developing ways to increase the insulin-releasing function of beta cells and maintain the patients’ left-over insulin-secreting beta cells.

Based on this goal, my mentor’s lab and other labs have examined the option for the enrichment of a protein named “DOC2b”, which is important for the controlled release of insulin from beta cells. Our recent studies showed that increasing the amount of DOC2b in beta cells proportionately improves their insulin secreting function, thus making each beta cell more efficient. DOC2b enrichment can also restore the malfunctioning islets (from diabetic humans) to normal islets in petri dishes. Additionally, these beta cells keep their normal insulin production and do not exhaust/ fail. This points towards the exciting possibility that DOC2b plays a role in beta cell survival.

My goal for this project is to discover the methods to increase the DOC2b protein levels in existing insulin-producing beta cells in T1D patients and to study if DOC2b enriched beta cells can resist the damages associated with T1D in living mammals. By pursuing these studies, I will address one very important question: could DOC2b enrichment be a method to preserve and restore the function of human beta cells? If found to be true, this would be significant progress toward the treatment of T1D.