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Funded Research

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    • 2004
      The Professor David Matthews Non-Clinical Fellowship

      Investigation of glucose sensing in the brain.

      Recipient:
      Dr Gavin Bewick
      Institution:
      Imperial College London
      City:
      London
      Amount:
      £164,189.32
      Description: The complications of diabetes are the result of poor glycaemic control, which can be prevented by intensive insulin therapy. However, this therapy is limited by hypoglycaemia and the subsequent loss o...
      Description: The complications of diabetes are the result of poor glycaemic control, which can be prevented by intensive insulin therapy. However, this therapy is limited by hypoglycaemia and the subsequent loss of normal counter regulatory responses. Indeed hypoglycaemia is reported to account for 18% of deaths for type I diabetic subjects. A region of the brain called the hypothalamus is the key site controlling the counter regulatory response to hypoglycaemia. Glucokinase is the body’s glucose sensor and is expressed at high levels in specialised glucose sensing neurones in the hypothalamus. Their activity is modulated by alterations in glucose concentrations and controls the counter regulatory response to hypoglycaemia. I hypothesize that alterations in glucokinase function in glucose sensing neurones underlie the development of a defective counter regulatory response to hypoglycaemic in diabetics. To establish the role of glucokinase in the counter regulatory response I will both increase and decrease glucokinase function in the hypothalamus using the gene therapy vector adeno-associated virus. The effect of altered glucokinase function on glucose homeostasis and the counter regulatory response to hypoglycemia will be determined in the non diabetic state and in a model of Type 1 diabetes. This work will establish the neurones critical to the prevention of hypoglycaemia which limits fully successful insulin therapy and results in significant additional morbidity for insulin deficient diabetic subjects and is the first stage to identifying ways to improve the response to hypoglycaemia.
    • 2003
      Research Grant, Open Funding

      Adapting the HOMA model to estimate insulin sensitivity and beta cell function in people with Type 2 diabetes mellitus treated with insulin

      Recipient:
      Prof. Rury Holman/Dr Richard Stevens
      Institution:
      University of Oxford
      City:
      Oxford
      Amount:
      £29,983
      Description: "Blood glucose levels depend on how much insulin the body can make, and how the body responds to insulin. These can be estimated simply with a blood sample and the HOMA computer program. Curren...
      Description: "Blood glucose levels depend on how much insulin the body can make, and how the body responds to insulin. These can be estimated simply with a blood sample and the HOMA computer program. Currently, HOMA does not work for people with diabetes who take insulin. This project will produce a new version to make this possible. This will be used by researchers, developing treatments for diabetes."
    • 2003
      Research Grant, Open Funding

      Finding the genes in human adipose tissue that cause insulin resistance

      Recipient:
      Prof. Peter Arner/Prof. Keith Frayn
      Institution:
      Karolinska Institute/Oxford
      City:
      Oxford
      Amount:
      £30,000
      Description: Professors Arner and Frayn have performed microarrays on human adipose tissue of lean and obese subjects and found a novel gene strongly associated with insulin resistance. The function of this gene ...
      Description: Professors Arner and Frayn have performed microarrays on human adipose tissue of lean and obese subjects and found a novel gene strongly associated with insulin resistance. The function of this gene in human fat cells is currently under investigation.
    • 2003
      Sutherland-Earl Clinical Fellowship

      Is the abnormal postprandial suppression of hepatic glucose production in type 2 diabetes reversible by decreasing intrahepatic triglyceride stores?

      Recipient:
      Dr B. Ravikumar
      Institution:
      University of Newcastle
      City:
      Newcastle
      Amount:
      £100,000
      Description: The liver usually produces glucose as needed by the body. This production is normally stopped after meals. However, in type 2 diabetes, the liver fails to stop producing glucose and this adds to the...
      Description: The liver usually produces glucose as needed by the body. This production is normally stopped after meals. However, in type 2 diabetes, the liver fails to stop producing glucose and this adds to the glucose absorbed from food, causing higher blood glucose levels. Previous research has shown that the impaired regulation of glucose controlling hormones (insulin and glucagon) and excess fat stored in the liver are responsible for this increased glucose production. We aim to investigate the relative importance of the hormones and the hepatic fat content on the regulation of glucose production. By using a combination of tablets to reduce hepatic fat content, we will examine whether this reduces glucose production. In a separate study, we will use an experimental hormone infusion to normalise the glucose controlling hormones and study its effect on glucose production. Finally, the effect of these factors will be examined in people with impaired glucose tolerance, a condition that precedes the development of overt diabetes.
    • 2003
      Research Grant, Open Funding

      The role of Synaptotagmins in Insulin-stimulated Glucose Transport in the Adipocyte

      Recipient:
      Dr Steven Miller
      Institution:
      University of Glasgow
      City:
      Glasgow
      Amount:
      £27,000
      Description: The role of Synaptotagmins in Insulin-stimulated Glucose Transport in the Adipocyte...
      Description: The role of Synaptotagmins in Insulin-stimulated Glucose Transport in the Adipocyte

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