In diabetes, insulin-producing beta cells are either destroyed or stop working properly. Professor Persaud will investigate the role of a protein found on beta cells in improving the effectiveness of islet transplants and increasing beta cell numbers. This could lead to new and improved treatments for both Type 1 and 2 diabetes.
Background to research
In Type 1 diabetes, insulin-producing beta cells in the pancreas are destroyed by the immune system. Beta cells are found in small regions of the pancreas called islets. Some people with Type 1 diabetes can receive an islet transplant, but there are few donors available and the cells don’t survive long-term.
In Type 2 diabetes, the same cells stop working properly and aren’t able to produce enough insulin. The body will attempt to make up for this by trying to make more insulin, but over time this can cause beta cells to wear out.
Professor Persaud and her team have already found a protein on beta cells, called GPR56, and shown that insulin production is higher when it’s activated. Professor Persaud has also found that new-born mice, that don’t have any GPR56 proteins, have fewer beta cells and smaller islets.
Professor Persaud wants to explore these findings further and carry out a thorough investigation around GPR56 in islets. Using islets from mice and human donors, the team will look at whether GPR56 can improve the survival of islets after transplantation in Type 1 diabetes.
In Type 2 diabetes, Professor Persaud wants to find out what role GPR56 plays in allowing the body to make more beta cells, to help people with Type 2 produce enough insulin to manage their blood glucose levels without medication.
Potential benefit to people with diabetes
In the shorter-term, this work could be used to improve the effectiveness of islet transplants for people with Type 1 diabetes. In the longer-term, it could lead to the development of new treatments for people with Type 2 diabetes that help the body make more working beta cells.