- 2020Pump Priming
Novel genetic insights into autoimmune diabetesRecipient:Dr Matthew JohnsonInstitution:University of ExeterCity:ExeterAmount:£19,600Description: We do not fully understand how destruction (autoimmunity) of the insulin-producing cells in the pancreas develops in type 1 diabetes (T1D). A condition which is very similar to T1D, and much easier to study, is monogenic autoimmune diabetes which is caused by a single letter change (a mutation) in an individual’s DNA. Studying patients with monogenic diabetes will provide new insights into how insulin-producing cells are destroyed which will increase understanding of T1D. We will use a powerful genetic technique (genome sequencing) to find the single letter change that is causing destruction of the insulin-producing cells in individuals with suspected monogenic autoimmune diabetes providing a genetic diagnosis to the families. Furthermore, these findings will identify new biological pathways which are responsible for the development of autoimmunity that will have important implications for patients with more common type 1 diabetes.
- 2019Pump Priming
Investigating the role of Viperin in beta cells as a mechanistic link between enteroviral infection and the development of type 1 diabetesRecipient:Dr James CantleyInstitution:University of OxfordCity:OxfordAmount:£20,000Description: 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).
- 2019Pump Priming
A James Lind Alliance Priority Setting Partnership to define the research priorities in diabetes and pregnancyRecipient:Dr Goher AymanInstitution:University of OxfordCity:OxfordAmount:£19,567Description: Diabetes affects over 5% of all women giving birth in the UK. It increases the risk of complications during pregnancy and birth for the mother and her baby, and can also affect them in the long-term. More research is needed to help provide the best health care for women with or at risk of diabetes, who are planning or are pregnant. This project aims to help direct the research which is done in diabetes and pregnancy towards addressing the areas which are considered most important by the people impacted by it. Over approximately 12-18 months we will work with women and their families affected by diabetes in pregnancy, and health care professionals, to identify where little is known, or there are uncertainties about, the effects of treatments and health care in diabetes and pregnancy. A top ten list of priority research questions will be jointly agreed and shared with the public and research funders. Where possible, research projects will be developed and submitted for funding.
- 2019Pump Priming
Defining the role of chemokine receptor CCR9 in islet function: potential for therapeutic intervention in type 2 diabetesRecipient:Dr Patricio AtanesInstitution:King’s College LondonCity:LondonAmount:£19,995Description: 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.
- 2019Pump Priming
RNA binding proteins (RBP) and insulin secretion: an unexplored area of diabetes researchRecipient:Professor Terence HerbertInstitution:University of LincolnCity:LincolnAmount:£19,005Description: Specialised cells called beta-cells make and release the hormone insulin which reduces the levels of sugar in the blood. Diabetes occurs when these cells fail to secrete enough insulin leading to raised blood sugar. We have discovered, in beta cells, a new set of proteins that we have named ‘secretory RBPs’. We believe that these novel proteins play a vital role in making and releasing insulin and may play an important role in causing the beta cells to ‘fail’. With the generous support of the DWRF we wish to follow up this exciting discovery to find out more about the role of these secretory-RBPs’ in beta cells. This will lead to a better understanding of how the insulin is made and released and what causes the beta cell to stop working as it does in people with diabetes. We anticipate that the results of the project will ultimately lead to the development of new treatments for the prevention and management of diabetes.