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Funded Research

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  • 2018

    A role for hypothalamic hormones in the islet adaptation to pregnancy

    Recipient: Dr James Bowe
    Institution: King’s College London
    City: London
    Funding Type: Pump Priming
    Amount: £17,782
    Description: During healthy pregnancy insulin sensitivity in the mother decreases and the insulin-secreting beta-cells in the islets of Langerhans release more insulin and increase in number to maintain normal blood glucose levels. Gestational diabetes mellitus (GDM) is a form of diabetes that occurs specifically during pregnancy and occurs when the maternal islets are unable to sufficiently compensate for the increased insulin resistance, though the mechanisms involved are currently poorly understood. Corticotropin releasing hormone (CRH) and growth hormone releasing hormone (GHRH) are two hormones that are primarily released from the hypothalamic area of the brain. They are responsible for controlling stress responses and growth respectively. Both hormones also have beneficial effects on the beta-cells, though the physiological reason for this is unknown. Levels of CRH and GHRH in the blood are low under most circumstances, but increase greatly during pregnancy due to release from the placenta. Thus, this project will investigate whether CRH and/or GHRH regulate beta-cell adaptation to pregnancy, and whether insufficient CRH or GHRH is linked to GDM.
  • 2018

    Bringing immunotherapy for type 1 diabetes into the clinic: new windows into the immune response

    Recipient: Dr Danijela Tatovic
    Institution: Cardiff University
    City: Cardiff
    Funding Type: Pump Priming
    Amount: £19,550
    Description: Type 1 diabetes (T1D) is caused when cells of the immune system called T-cells attack and destroy insulin producing cells in the pancreas. Monitoring of these pivotal immune cells is currently highly challenging as we cannot see what is happening in the pancreas. I have developed ways to monitor T-cell activity by studying organs called lymph nodes that act as ‘stations’on the transport network that T-cells use to travel around the body. These lymph nodes provide a window into what is happening in the pancreas during disease and allow monitoring of events during clinical trials. The technique I developed involves the use of a very fine needle that is guided using ultrasound. I now wish to use it to monitor the T-cells responsible for killing to insulin-producing cells using stateof-the-art technologies developed by my collaborators who are world leading experts in T-cells during T1D. This pump priming funding will allow me to establish important new collaborations aimed at monitoring T-cells during immunotherapy trials.
  • 2018

    Cx43 mediated regulation of the inflammasome, a therapeutic target in diabetic nephropathy

    Recipient: Dr Claire Hills
    Institution: University of Lincoln
    City: Lincoln
    Funding Type: Pump Priming
    Amount: £19,170
    Description: Cells lining the surface of the small tubes of the kidney work together to ensure that appropriate function is maintained. However, in the diabetic kidney, these cells become bathed in high levels of sugar and associated stress molecules that affect kidney cell behavior. We have previously demonstrated that high sugar reduces stickiness between kidney cells, an event that impairs the way in which cells talk to each other, and ultimately affects their ability to work efficiently. More importantly, our preliminary studies suggest, that in kidneys of people with diabetic nephropathy, there are altered levels of proteins responsible for transferring information between both cells and their surrounding environment. In the absence of appropriate data sharing, cells respond inappropriately to incoming danger changes and ultimately kidney function is impaired. Our proposal aims to understand the mechanisms which link inappropriate cell conversation to the damage that occurs in the diabetic kidney. Importantly, in collaboration with our clinical colleagues, we will demonstrate the ability of a new therapeutic to negate these effects.
  • 2018

    Defining heterogeneity of clinically diagnosed adult-onset type 1 diabetes using genetic and islet autoantibodies

    Recipient: Dr Kashyap Patel
    Institution: University of Exeter Medical School
    City: Exeter
    Funding Type: Pump Priming
    Amount: £18,581
    Description: Half of all type 1 diabetes develops in adulthood. Half of these patients are misdiagnosed and therefore potentially treated incorrectly. This is due to both lack of tools to confirm type 1 diabetes at diagnosis and overlapping features with other subtypes of diabetes (type 2 diabetes and monogenic diabetes, a rare familial diabetes due to mutation in a single gene). This study will analyse whether the combination of currently used blood tests (islet autoantibodies) and a new DNA–based tool (type 1 diabetes genetic risk score, T1D-GRS) can reduce misdiagnosis. We will measure the efficacy of these tools in 700 people with clinically diagnosed adult-onset type 1 diabetes (age at diagnosis 20-80 years). Genetic tests will be used to identify misdiagnosed monogenic diabetes. This study will provide a framework for the accurate diagnosis of adult-onset T1D in routine clinical practice. The study will also be the first to provide an estimate of misdiagnosed monogenic diabetes, resulting in patients getting the correct treatment and better care.
  • 2018

    Increasing beta-cell mass in type 2 diabetes: Does reduced NAD supply result in loss of beta-cell identity in T2D?

    Recipient: Dr Paul Caton
    Institution: King’s College London
    City: London
    Funding Type: Pump Priming
    Amount: £20,000
    Description: Type 2 diabetes develops in part due to low levels of insulin release from pancreas. Previous work has shown that this can happen in type 2 diabetes because the insulin producing beta-cells change into different cell types, resulting in lower insulin secretion. This means that if we can learn how to stop beta-cells changing into other cells, or convert changed cells back to beta-cells, this could lead to the development of new drugs to treat or prevent type 2 diabetes. This study will build on our previous work to investigate whether a particular factor, called NAD, plays an important role in stopping insulin producing cells converting into other cells. If successful, new approaches which boost levels of NAD could be used as drugs to treat or prevent type 2 diabetes.