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Funded Research

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  • 2015

    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 diabetes

    Recipient: Dr Richard Metcalfe
    Institution: Ulster University
    City: Ulster
    Funding Type: Pump Priming
    Amount: £12,260
    Description: 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
  • 2015

    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 West
    Institution: Newcastle University
    City: Newcastle
    Funding Type: Pump Priming
    Amount: £19,470
    Description: 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.
  • 2015

    CD4 T cell differentiation markers as predictors of type 1 diabetes development and progression

    Recipient: Professor Lucy Walker
    Institution: UCL Institute of Immunity & Transplantation
    City: London
    Funding Type: Pump Priming
    Amount: £20,000
    Description: 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
  • 2015

    Mechanisms and prognostication of type 2 diabetes resolution following bariatric surgery

    Recipient: Mr Nicholas Penney
    Institution: Imperial College London
    City: London
    Funding Type: Sutherland-Earl Clinical Fellowship
    Amount: £209,164
    Description: Bariatric (weight loss) surgery is currently the most successful treatment for obesity. Bariatric surgery has also emerged as a highly effective treatment of type 2 diabetes in obese patients, rapidly reducing and often removing the need for patients to take diabetic medications. Interestingly, the improvement in patients’ diabetes after bariatric surgery occurs long before any significant weight loss. Through a better understanding of the reasons behind this, bariatric surgery can provide a unique 'looking glass' to identify new, non-surgical ways of treating diabetes and obesity. Recent studies have shown that bacteria within the gut play an important role in the improvement seen in patients’ diabetes. Bariatric surgery fundamentally changes the environment within the gut, which results in changes to the makeup of the trillions of bacteria living within it. These changes in the gut bacteria can affect the body in a number of complex ways, which we are only just beginning to understand. For example, gut bacteria breakdown food we are unable to absorb ourselves, leading to altered sugar levels and can release molecules that act to increase insulin sensitivity or reduce appetite. In this study I aim to characterise the changes that occur to the gut bacteria after bariatric surgery and gain a better understanding of how these changes lead to an improvement in diabetes. With this understanding I hope to discover potential targets for future treatments, such as identifying beneficial gut bacteria that could be supplemented with probiotics in patients. Additionally, although bariatric surgery is a highly successful treatment, approximately 30% of obese patients do not undergo a significant improvement in their diabetes after surgery. I aim to identify molecules (metabolites) within the patient's blood or urine that are able to predict the likely chance a patient will undergo improvement in their diabetes after bariatric surgery. This will help doctors and patients assess the likely benefit from bariatric surgery, thus enabling a personalised approach towards patient care.
  • 2015

    The mechanisms linking glucose sensing to autophagic flux in pancreatic beta-cells

    Recipient: Dr Catherine Arden
    Institution: Newcastle University
    City: Newcastle
    Funding Type: Pump Priming
    Amount: £19,715
    Description: Type 2 diabetes (T2DM) occurs when the insulin-releasing beta-cells of the pancreas fail to secrete sufficient insulin, a consequence of decreased insulin release and decreased cell number. The purpose of the proposed work is to explore a role for autophagy in the regulation of beta-cell number. Autophagy is a recycling system that uses damaged cell components to provide energy in response to changes in fuel availability, and can either act to promote cell survival or cell death. The aim of the proposed study is to explore how beta-cells regulate autophagy in response to changes in glucose concentration. We will explore how beta-cells alter their cell recycling mechanism in response to both acute and chronic changes in glucose levels and investigate the cellular mechanisms involved. The data generated by this pilot study will provide the basis for future large scale grant applications investigating the molecular links between glucose-sensing and autophagy in beta-cells and how these pathways impact on beta-cell number in T2DM