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Funded Research

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    • 2018
      Pump Priming

      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
      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 a...
      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
      The Professor David Matthews Non-Clinical Fellowship

      Improving islet transplantation outcomes by harnessing the mesenchymal stromal cell secretome to target the donor islet graft and host environment

      Recipient:
      Dr Chloe Rackham
      Institution:
      King’s College London
      City:
      London
      Amount:
      £194,934
      Description: This research aims to define the mechanisms though which Mesenchymal Stromal Cells (MSCs) or the biologically active substances that they produce should be used to improve the efficiency of clinical i...
      Description: This research aims to define the mechanisms though which Mesenchymal Stromal Cells (MSCs) or the biologically active substances that they produce should be used to improve the efficiency of clinical islet transplantation. Our experiments have shown that MSCs produce Annexin A1 (ANXA1) and that ANXA1 partially mimics the beneficial effects of using MSCs. We aim to define a 'cocktail' of therapeutic factors produced by MSCs, that can be used instead of the MSCs, to fully reproduce the beneficial effects of MSCs in transplantation protocols. Defining MSC-derived biotherapeutics will allow simple modifications to clinical transplantation, that will help to overcome some of the safety concerns of using MSCs directly and allow safe and reproducible modifications to be carried out. The proposed work will help design and start a clinical trial within the next five years. Through improving the efficiency of the transplant procedure, clinical islet transplantation can be offered as a therapeutic option to the greatest possible number of patients with Type 1 Diabetes and improve outcomes for individual transplant recipients.
    • 2018
      The Professor David Matthews Non-Clinical Fellowship

      Improving islet transplantation outcomes by harnessing the mesenchymal stromal cell secretome to target the donor islet graft and host environment

      Recipient:
      Dr Chloe Rackham
      Institution:
      King’s College London
      City:
      London
      Amount:
      £194,934
      Description: This research aims to define the mechanisms though which Mesenchymal Stromal Cells (MSCs) or the biologically active substances that they produce should be used to improve the efficiency of clinical i...
      Description: This research aims to define the mechanisms though which Mesenchymal Stromal Cells (MSCs) or the biologically active substances that they produce should be used to improve the efficiency of clinical islet transplantation. Our experiments have shown that MSCs produce Annexin A1 (ANXA1) and that ANXA1 partially mimics the beneficial effects of using MSCs. We aim to define a 'cocktail' of therapeutic factors produced by MSCs, that can be used instead of the MSCs, to fully reproduce the beneficial effects of MSCs in transplantation protocols. Defining MSC-derived biotherapeutics will allow simple modifications to clinical transplantation, that will help to overcome some of the safety concerns of using MSCs directly and allow safe and reproducible modifications to be carried out. The proposed work will help design and start a clinical trial within the next five years. Through improving the efficiency of the transplant procedure, clinical islet transplantation can be offered as a therapeutic option to the greatest possible number of patients with Type 1 Diabetes and improve outcomes for individual transplant recipients.
    • 2018
      Pump Priming

      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
      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 int...
      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.
    • 2018
      Pump Priming

      New insights into development and function of human beta-cells by gene discovery in early-onset diabetes

      Recipient:
      Dr Elisa De Franco
      Institution:
      University of Exeter Medical School
      City:
      Exeter
      Amount:
      £20,000
      Description: We need to understand more about how the insulin-producing beta-cell works. One good way to do this is to study patients who get diabetes because they do not make insulin as a result of a single spell...
      Description: We need to understand more about how the insulin-producing beta-cell works. One good way to do this is to study patients who get diabetes because they do not make insulin as a result of a single spelling mistake in one word of their whole library of books of genetic information (monogenic diabetes). These patients are likely to develop diabetes when young. We will look for the genetic cause of diabetes in patients diagnosed between 6-12 months using two recently available tools: 1) a test which allows us to select patients likely to have monogenic diabetes, this is called a genetic risk score; 2) whole-genome-sequencing which allows us to analyse the entire human DNA to identify the critical spelling mistakes in the genetic information. Using these tools we will identify the likely cause of diabetes in these children and confirm it in other patients. As we have already excluded the known causes of monogenic diabetes, this will be a new finding which will help us to understand the beta-cell better.

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