Funded Research

We want to understand the role of Viperin, a protein that the body makes as part of the immune response to viral infection, in the development of type 1 diabetes (T1D). As viral infection of the insulin-producing pancreatic beta cells has been linked to the onset of T1D, we want to understand if Viperin plays a role in this process. This knowledge may enable the development of drugs/treatments to prevent or intervene early in the disease, potentially avoiding many of the severe complications of T1D such as diabetic ketoacidosis. In particular, we want to find out: 1) How much Viperin people with recent-onset T1D have in their pancreas. 2) How much Viperin there is in a human pancreatic beta cell model (cell line maintained in a test tube) infected with virus (like a person developing T1D). 3) The role played by Viperin in beta cell dysfunction and death, using cell models relevant to T1D (cells infected with virus or exposed to proteins called cytokines produced by the immune system).

Type 2 diabetes (T2D) occurs when blood sugar (glucose) levels are too high because the specialised islet beta-cells do not release enough insulin, or insulin does not work properly. T2D can be treated by drugs that stimulate insulin secretion but some patients cannot properly regulate their glucose levels using these therapies and may suffer from side effects. Some chemicals regulate beta-cell health and function by binding to "receptor" proteins. We know that obesity stresses beta-cells and we have identified that islet cells from obese organ donors show alterations in the amounts of particular receptors that they contain. We are particularly interested in a receptor called CCR9, which is nearly 100-times more abundant in islets from obese donors than islets from normal weight donors. In this small project we will investigate whether this increase in CCR9 has a protective function or is involved in the beta-cell damage associated with obesity. This study will therefore provide essential feasibility information for further development of drugs targeting CCR9 to treat T2D.

Significant weight loss (>10kg) can help a large majority of people to come off their medications and achieve remission of their type 2 diabetes. However, for many people, weight loss might not be possible or desired. Promising studies show that low-carbohydrate diets can reduce blood sugar to the level of someone without type 2 diabetes without any weight loss. However, these low-carbohydrate diets also included a lot of high-protein foods. Protein might help the pancreas produce more insulin. Therefore it is not clear whether carbohydrate restriction alone is enough to normalise blood sugar. This study will test the effect of changing the amount of protein in the diet while people are on a low-carbohydrate diet in people with and without type 2 diabetes. We will increase and decrease the protein in random order but keep the carbohydrate intake unchanged to see what happens to blood sugar levels. This will tell us if added protein is specifically needed for carbohydrate restriction to lower blood sugar in people with type 2 diabetes.