Funded Research
Our annual funding round is designed to support bright young researchers, as well as established institutions, as they strive to make the kind of life-changing breakthrough our diabetes community is hoping for.
Our first research award was made in 1999 for a small equipment grant and since that time, we have committed more than £12 million to diabetes research in the UK and as part of the International Diabetes Wellness Network, around the world.
To read more about our research strategy, click here.
2004
Pump Priming
Diabetic nephropathy
Recipient: Dr Andrew Advani
Institution: University of Newcastle
City: Newcastle
Amount: £9,000
- Description - click here to read
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This project seeks to answer the question of whether a new drug that stops the way the Urotensin II protein works can prevent the development of diabetic kidney disease. Diabetes is the most common cause of kidney failure in the Western world and current drug treatments to prevent kidney failure in diabetes, such as tablets called ACE inhibitors, are only partly successful. New drug treatments are therefore needed and this project will provide important evidence in the development of new drugs. This project seeks to answer the question of whether a new drug that stops the way the Urotensin II protein works can prevent the development of diabetic kidney disease. Diabetes is the most common cause of kidney failure in the Western world and current drug treatments to prevent kidney failure in diabetes, such as tablets called ACE inhibitors, are only partly successful. New drug treatments are therefore needed and this project will provide important evidence in the development of new drugs.
2004
Pump Priming
Diabetic retinopathy
Recipient: Dr Stephen Aldington
Institution: Imperial College London
City: London
Amount: £21,252
- Description - click here to read
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Diabetic retinopathy remains the most common cause of blindness in the UK in the working age population. The most common reason for loss of sight as a result of diabetic retinopathy is the development of macular oedema. Macular oedema is the swelling or water-logging of the macular area of the eye (the macula is a small circular area of the retina that provides our central detailed vision) caused by an accumulation of abnormal fluid in and around the macula and associated fat (lipid) deposits called hard exudates. In this small study the researchers intend to use photographs of the retina from a completed study called the UKPDS to investigate whether patients who have these hard exudates located physically above the centre of the macula (a point called the fovea) are more likely to eventually suffer from loss of sight than those in whom the hard exudates are located only below or to the side of the fovea. The researchers believe that it is the effect of gravity on the hard exudates and abnormal fluid located directly above the fovea that is responsible for seriously affecting central vision. Patients who have hard exudates only below or to the side of the fovea are thought to be less likely to suffer from future loss of central sight, as the effect of gravity in these cases would tend to draw the fluid and hard exudates away from the fovea. These patients therefore may not require invasive laser treatment. If the study is shown to be correct in its assumptions it will provide an extremely useful tool in the screening of patients with diabetes for retinopathy in terms of likely outcome and treatment needed.
2004
Pump Priming
Human Islet Isolation Facility
Recipient: Islet Transplantation Programme
Institution: OCDEM Oxford
City: Oxford
Amount: £1,200,000
- Description - click here to read
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Diabetes Research & Wellness Foundation recently granted an unprecedented £1.2million to islet transplantation research. The award, the largest of its kind in the UK, was made to the Oxford Consortium for Islet Transplantation (OXCIT), whose highly regarded team of researchers is spearheading the search for a cure. Housed in the new state-of-the-art Oxford Centre for Diabetes, Endocrinology & Metabolism (OCDEM), a new islet isolation facility will be built with the donation from DRWF. The OCDEM project, brainchild of the late Professor Robert Turner and Professor David Matthews, heralds a new concept in research and care.The development was only possible thanks to the unique partnership formed by the University of Oxford, the NHS and leaders in diabetes care from private industry. At the official launch of the OCDEM on 11 September 2003, the grant from DRWF was described as the "jewel in the crown."
2004
Pump Priming
Insulin resistance
Recipient: Dr Mimi Chen
Institution: University of Bristol
City: Bristol
Amount: £29,988
- Description - click here to read
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The mechanism by which an increase in weight causes insulin resistance is not known. When insulin binds to a cell, it produces a variety of proteins which help to activate a channel through which glucose enters the cell. In insulin resistance, binding of insulin does not cause glucose to enter the cell. Using a combination of sophisticated insulin infusions and a unique array of biochemical markers developed in Bristol, the research team aims to develop a technique capable of studying how insulin produces these proteins in the human body. This technique will then be used to study the changes in these proteins that occur when dramatic weight loss reduces insulin resistance. It is hoped the understanding of the proteins which link weight gain to insulin resistance gained using will lead to the development of new approaches to prevent the rising tide of Type 2 diabetes.
2004
Pump Priming
Insulin resistance and cardiovascular disease
Recipient: Dr Antonio Vidal-Puig
Institution: University of Cambridge
City: Cambridge
Amount: £5,700
- Description - click here to read
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This project is relevant to diabetes because it addresses how metabolic defects typically associated with diabetes promote cardiovascular problems. The objective is to investigate why diabetes is a cardiovascular risk factor and how it makes us more susceptible to myocardial infarction.
2004
Pump Priming
Insulin secretion
Recipient: Dr Luke Chamberlain
Institution: University of Glasgow
City: Glasgow
Amount: £29,928
- Description - click here to read
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This project will examine a previously unexplored area of insulin secretion. Understanding the mechanisms of insulin secretion is of prime importance for the treatment and potential cure of both Type 1 and Type 2 diabetes. It is essential to have a complete understanding of the mechanism of insulin secretion if future therapies for Type 1 diabetes are to be successful. Knowledge of the molecular control of insulin secretion is also essential for understanding beta cell dysfunction in Type 2 diabetes.
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 - click here to read
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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.
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