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  • 2016
    Pump 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 West
    Institution:
    Newcastle University
    City:
    Newcastle
    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 l...
    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.
  • 2016
    Pump Priming

    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
    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...
    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
  • 2016
    The Professor David Matthews Non-Clinical Fellowship

    Epigenetic changes in multi-generation type 1 diabetes families

    Recipient:
    Dr Jody Ye
    Institution:
    University of Bristol
    City:
    Bristol
    Amount:
    £179,774.00
    Description: Type 1 diabetes is caused when the immune system makes a mistake and destroys the insulin-secreting beta cells in the pancreas. We know that genes play an important role in causing the condition but f...
    Description: Type 1 diabetes is caused when the immune system makes a mistake and destroys the insulin-secreting beta cells in the pancreas. We know that genes play an important role in causing the condition but factors in our environment such as viral infections, pre-natal environment, and early nutrition are also thought to be important. Over recent decades, the incidence of type 1 diabetes has increased rapidly (~3% annually especially in children under 5 years of age). In addition, more people with less type 1 diabetes associated genes develop the condition today compared with previous generations. This suggests the increasing importance of environmental effects in type 1 diabetes. Unlike genes that are usually inherited unchanged from parents, DNA itself can be chemically modified, a phenomenon called DNA methylation. This process has been shown to be changed by environmental exposures and can be different in one individual to another. My collaborator, Professor Yaron Tomer and his team at Albert Einstein College of Medicine in New York has already shown that methylation differences can be found in identical twins where one twin was affected by type 1 diabetes while the other was not. In my three-year fellowship, I will travel to Professor Tomer’s laboratory to study multi-generation type 1 diabetes families from the Bart’s Oxford (BOX) family study of type 1 diabetes which has been running for over 30 years. I am going to investigate whether DNA methylation has changed in children with type 1 diabetes compared with their parents and grandparents. This study will allow us to find out whether the changing environment over time is associated with the increasing incidence of diabetes by modifying our DNA. We hope that this research will identify new markers that can be used in clinical trials to more accurately assign disease risk. In addition, we will dissect the underlying molecular mechanisms to uncover why environmental exposures trigger changes to the immune system leading to beta cell death. In the longer term, if we can understand why type 1 diabetes is becoming more common we may be able to intervene to delay or prevent the condition.
  • 2016
    Pump Priming

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

    Recipient:
    Dr Catherine Arden
    Institution:
    Newcastle University
    City:
    Newcastle
    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 purpos...
    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
  • 2016
    Pump Priming

    Understanding the relationship between lipid droplet pattern and mitochondrial function and morphology in human primary hepatocytes

    Recipient:
    Professor Leanne Hodson
    Institution:
    OCDEM
    City:
    Oxford
    Amount:
    £19,382
    Description: More people with type 2 diabetes have fatty liver disease than people without diabetes. Liver fat accumulation (steatosis) consists of either a large number of small (microsteatosis) or one large (mac...
    Description: More people with type 2 diabetes have fatty liver disease than people without diabetes. Liver fat accumulation (steatosis) consists of either a large number of small (microsteatosis) or one large (macrosteatosis) fat (lipid) droplet within liver cells (hepatocytes). Large lipid droplets are thought to interfere with the part of the cell that produces energy (mitochondria) so that they don’t work efficiently. We will investigate the relationship between lipid droplets and mitochondrial function in human liver cells. Liver tissue will be obtained from patients undergoing surgery and from this hepatocytes will be isolated. We will then measure the size and number of the lipid droplets and their localisation to mitochondria, using a state-of-the-art automated imaging machine. We will also assess the health and function of the mitochondria by determining their ability to produce energy. This work will help us to understand the relationship between fat in the liver and mitochondrial function and also provide information about pathways that new drugs could be developed for to help to keep the liver healthy

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