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.
2005
Research Grant, Open Funding
Development of a device to prevent or reverse diabetic retinopathy
Recipient: Prof Geoffrey Arden
Institution: City University London
City: London
Amount: £12,000
- Description - click here to read
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Although the treatment of diabetes with insulin or other drugs is quite successful, the complication of diabetic retinopathy ( DR) is still intractable. It develops insidiously, and leads to rapid loss of vision. Very close control of blood sugar levels can slow the rate of progress down, but still over 75% of diabetic persons of 15 years standing develop this condition. Expensive screening methods are only partially successful. Surgical treatment is invasive and destructive and therefore can only be employed in fairly advanced cases: it is not always successful. Great effort has recently been expended in developing drugs to prevent the condition developing or progressing. This focuses on the recent consensus that there is a substance called VEGF that is produced in excess in the retina of people with diabetes, and this is the cause of DR. Early reports suggest that these drugs work, but they have serious disadvantages. They must be injected, every few weeks, directly into the eyeball by doctors as a special procedure. There are serious side effects, and the drugs are also costly. The applicant has suggested an alternative method of treatment- to remove the conditions that cause the production of VEGF by continuously and mildly light-adapting the eye during sleep. Small trials to provide proof of the principle are under way but large scale trials require the construction of an electronic “light mask” before they can be authorized. Funding for design and initial production is required.
2005
Research Grant, Open Funding
Endothelin receptor antagonism as a therapeutic target in diabetic nephropathy
Recipient: Dr Neeraj Dhuan
Institution: University of Edinburgh
City: Edinburgh
Amount: £29,061
- Description - click here to read
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Diabetes is the most common cause of kidney failure in the developed world. Patients with diabetic kidney disease have higher blood pressures and lower blood flow to the kidneys than the general population. They also have stiffer blood vessels and more heart disease. The presence of protein in the urine suggests deteriorating kidney function and an increased risk of heart disease. If we are to tackle diabetic kidney disease effectively not only do we need to manage the problems with kidney function but also the heart disease with which they are associated. In this research, we wish to build on previous work that looked at a chemical produced by blood vessels called endothelin. Using endothelin blocking strategies we hope to show whether we can reduce blood pressure and blood vessel stiffness, increase blood flow to the kidneys, and decrease the amount of protein in the urine of individuals with diabetic kidney disease. If encouraging, these experiments may lead to future treatments that slow the progression of diabetic kidney disease and reduce the associated heart problems.
2005
Studentship
Glucokinase in Specialised Glucose-Sensing Neurones in Brain Plays a Key Role in Controlling Blood Glucose
Recipient: Mr Mayowa Osundiji
Institution: School of Clinical Medicine, Addenbrooke's Hospital
City: Cambridge
Amount: £51,000
- Description - click here to read
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Glucokinase (GK) is a specialised protein used in the pancreas to sense changes in blood glucose. It acts as a “gate” controlling the amount of glucose flowing into glucose-sensing pathways. It is also found in brain areas which sense low blood glucose (hypoglycaemia). In this studentship, Mayo Osundiji will use pharmacological blockers of GK delivered into brain of conscious free moving rats to examine the importance of brain GK in detecting hypoglycaemia and triggering the body’s defensive responses to hypoglycaemia (stimulation of hunger and release of anti-insulin hormones). Some patients with type 1 diabetes lose these protective responses putting them at an increased risk of suffering episodes of severe hypoglycaemia. Mayo will also examine whether blocking brain GK might help restore protective responses to hypoglycaemia. Finally, he will examine whether brain GK plays a wider role in controlling blood glucose and the sensitivity of tissues outside the brain such as fat and muscle to the glucose lowering effects of insulin. If this is true, brain GK might also represent a pharmacological target for reducing insulin resistance in type 2 diabetes- although probably in this case by increasing the activity of GK.
2005
Research Fellowship
Mapping novel type 1 diabetes genes in the major histocompatibility complex
Recipient: Dr Sergey Nezhentsev
Institution: Cambridge Institute for Medical Research
City: Cambridge
Amount: £118,126
- Description - click here to read
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Type 1 diabetes is a complex immune-mediated disease with strong genetic susceptibility. Genes located in the Major Histocompatibility Complex (MHC) on human chromosome 6 are its major genetic determinants. Previous research has shown that MHC contains an uncharacterised type 1 diabetes gene. The present study will localise this gene and analyse a new type 1 diabetes-associated molecule. It will improve our understanding of the disease pathogenesis and open new possibilities for genetic prediction of type 1 diabetes.
2005
Research Grant, Open Funding
Mechanisms of Schwann cell dysfunction under hyperglycaemia and in a mouse model of diabetic neuropathy.
Recipient: Dr Aviva Tolkovsky
Institution: University of Cambridge
City: Cambridge
Amount: £29,954
- Description - click here to read
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Diabetic neuropathy develops in 50% of diabetic patients. It is characterised by debilitating pain or loss of sensation, and can lead to gangrenous foot infections and amputation. There are no treatments for the neuropathic state. Schwann cells are crucially involved in supporting the neurons affected in diabetic neuropathy but little is known about why their responses go awry in the disease process. We have found that hyperglycaemia (high glucose concentrations commonly found in diabetes, especially when poorly controlled) profoundly inhibits the ability of Schwann cells to divide after nerve injury and thus repopulate regenerating nerve axons in culture. This proposal aims to reveal the molecules that mediate this loss of function by studying the cells in culture and in the context of a mouse model of diabetic neuropathy. Our study should enable better treatments to be developed to treat this incapacitating and ill-understood neuropathy.
2005
Pump Priming
The influence of glucose tolerance status on the predisposition to ex vivo thrombus formation of flowing blood and the effect of improving glycaemic control
Recipient: Dr Arun Natarajan
Institution: University of Newcastle
City: London
Amount: £40,977
- Description - click here to read
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The majority of individuals with type 2 diabetes die of heart attacks and strokes which are caused by clots in blood vessels. Several abnormalities in the blood cells and components involved in clotting, all of which increase the propensity to form clots, have been described in patients with diabetes. It is thought that these abnormalities may be responsible for the increased risk of clots in them. Evidence for this though, comes mainly from laboratory blood tests and the true impact of these abnormalities on actual clot formation within live blood vessels has not been fully explored. High blood glucose levels are characteristic of diabetes, but their impact on heart attacks and strokes remains controversial. We plan to quantify actual blood clots by passing blood through an experimental model (Badimon chamber). This model closely mimics the conditions present in a narrowed heart blood vessel which lead to clot formation. We will perform a number of laboratory tests of blood clotting and can thus determine their relation to the tendency to form clots. We will also study diabetic patients with high blood sugar levels before and after treatment with insulin, in order to assess the effects of blood glucose control on clot formation. Our study may therefore define the as yet unknown relation between the tendency for enhanced clot formation, blood components and blood glucose levels in patients with type 2 diabetes.
2005
Research Grant, Open Funding
The role of kisspeptin and its receptor GPR54 in pancreatic islet function
Recipient: Prof Peter Jones
Institution: King's College London
City: London
Amount: £29,878
- Description - click here to read
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Kisspeptin (KP) is a recently-discovered molecule that is only found in a few areas of the human body – the hypothalamic area of the brain, the placenta and the pancreas. One important function of KP in the brain is to control when the process of puberty starts, but the function(s) of KP in the placenta and the pancreas are unknown. We have shown that pancreatic KP is localised to the insulin-secreting ß-cells in islets of Langerhans, and that ß-cells also make receptors for KP, suggesting that KP is made and released with the islet to have a local regulatory effect. The hypothalamus, placenta and endocrine pancreas are all involved in the long-term regulation of energy balance so we propose that the ß-cell KP is involved in regulating islet function at times of changes in metabolic demand, such as starvation, obesity, pregnancy and Type 2 diabetes. The project will use existing techniques and reagents to measure the effects of KP on insulin secretion, and on the growth and survival of ß-cells. Information gained from these studies may identify new ways of modifying islet function (insulin secretion, ß-cell mass) with potential therapeutic applications.
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