- 2017Pump Priming
Role of adipose tissue ECM-integrin signalling in inflammation and insulin resistanceRecipient:Dr Li KangInstitution:University of DundeeCity:DundeeAmount:£19,859Description: Cells use glucose as fuel and the hormone insulin increases their use and removal of glucose from the blood. In Type 2 diabetes, cells do not respond normally to insulin and this causes increased blood glucose levels. We aim to develop a completely new way of improving cells response to insulin in people with diabetes. Up to now, work in this area has focused on studying how insulin affects mechanisms INSIDE cells. What makes our work different and exciting is that we study molecules OUTSIDE cells, the levels of which are increased when cells stop responding properly to insulin. This outside structural change is detected by proteins on the cell surface and so alters how insulin works. In this project, we will study a pathway that we believe is key to connecting the outside structural molecules to the cells response to insulin and so glucose removal from blood in fat tissues. We hope to develop these exciting results into new ideas for drugs for the benefit of people with diabetes.
- 2017Pump Priming
The role of microRNAs in transducing the programming actions of maternal obesity on beta-cell dysfunction in the offspring and exploring their use as biomarkersRecipient:Dr Lisa NicholasInstitution:University of Cambridge, Addenbrooke’s HospitalCity:CambridgeAmount:£19,860Description: The current global epidemic of obesity and type 2 diabetes (T2D) has been partly fuelled by the propagation of these diseases from parent to child across one or more generations. T2D develops when the function of insulin-secreting cells in the pancreas is impaired. Very few studies, however, have investigated underlying mechanisms within these cells that may explain transmission of T2D from mother to child. In recent years, there has been increasing interest in the role of epigenetics, which is the study of biological mechanisms that establish and maintain whether genes are switched on or off, in the development of T2D. This is largely due to the fact that unlike the genome of an individual, which is largely stable, the epigenome can be reversibly modified by exposure to nutritional and environmental factors e.g. obesity. The aim of this project is, therefore, to determine the impact of maternal obesity on the transmission of T2D risk to the offspring and to characterise epigenetic changes that may provide a mechanism for this event.
- 2016Pump Priming
A comparison of the acute impact of high-intensity interval training (HIT), reduced-exertion high-intensity interval training (REHIT) and moderate-intensity continuous aerobic exercise (MICE) on free-living glycaemic control in type 2 diabetesRecipient:Dr Richard MetcalfeInstitution:Ulster UniversityCity:UlsterAmount:£12,260Description: This research aims to determine whether a genuinely time-efficient exercise intervention is effective at improving the control of blood glucose in people with T2D. The exercise is based on high-intensity interval training (HIT), which utilises short bursts of vigorous exercise interspersed with periods of rest, but we have substantially reduced the number and length of the exercise intervals. Our protocol consists of 10-min of low intensity cycling with just two 20-second sprints in each session. Based on our previous work, this exercise mode is associated with low levels of exertion and fatigue, but is still effective at improving insulin function in sedentary men. However, it is not known if this type of exercise could improve blood glucose control in patients with T2D. We will: 1) investigate the effectiveness of this exercise to improve 24-hour glucose control; 2) compare the effects of this exercise mode with current exercise recommendations and another form of HIT; and 3) ask participants their perceptions of exertion, fatigue and enjoyment with each exercise mode
- 2016Pump Priming
Can residual beta-cell function predict glycaemic variability, inflammation and vascular repair at rest and after exercise in people with established type 1 diabetes?Recipient:Dr Daniel WestInstitution:Newcastle UniversityCity:NewcastleAmount:£19,470Description: When people with type 1 diabetes exercise, some experience hypoglycaemia, while others do not; in some HbA1c gets worse while in others it improves. Exercise is known to increase glucose variability leading to more time with high and low levels. It is now known that many people with long-standing type 1 diabetes can produce small amounts of insulin. It is unknown if this is important for limiting blood glucose variability at rest and around exercise. It is also unknown whether this low level of insulin impacts on important health markers such as how well blood vessels expand and shrink and how well the body can repair these vessels. We will examine the relationships between residual insulin production, glucose variability, blood vessel function and repair, inflammation and hypoglycaemia fear and incidence, at rest and after exercise. This will provide a foundation for larger studies which will look at how amount of residual insulin production could be used to predict the level of support people wishing to exercise may need.
- 2016Pump Priming
CD4 T cell differentiation markers as predictors of type 1 diabetes development and progressionRecipient:Professor Lucy WalkerInstitution:UCL Institute of Immunity & TransplantationCity:LondonAmount:£20,000Description: Type 1 diabetes is caused by immune cells called T cells, however it has not been clear which type of T cell is involved. We believe that a better understanding of this area will ultimately permit the development of new therapies to target the errant T cells and interrupt disease. We have recently discovered that a particular type of T cell, the follicular helper T cell (TFH) is overrepresented in people with type 1 diabetes. We think that measuring these cells could represent a new way to gauge the autoimmune response in people with this condition. This would have important implications for our ability to assess whether particular therapies are working and perhaps even help us to determine how likely a person is to develop diabetes in the first place. The current application builds on our recent findings and will shed light on how the number of these TFH cells changes in individual patients over time both before and after type 1 diabetes development