DRWF are pleased to announce that the following researchers have been awarded DRWF Open Funding grants for 2009. Each will last for a year.
Professor Gwyn Gould
Institution: Division of Biochemistry & Molecular Biology, Glasgow University
Amount: £29,747
Title: ‘Analysis of the role of Munc18c tyrosine phosphorylation in insulin-stimulated glucose transport’
Lay Summary: Insulin stimulates glucose transport into fat and muscle by promoting the movement of specialised transporter proteins from an internal storage depot to the cell surface. These transporter proteins function as specialised doorways through which glucose can move from the blood into fat and muscle for storage after a meal. By increasing the number of 'doorways' present in the boundary membrane of cells, insulin drives glucose into storage organs. This key action of insulin is known to be impaired in type 2 diabetes, resulting in insulin resistance and aberrant glucose homeostasis. This proposal is directed towards understanding how insulin controls the insertion of these doorways into the boundary membrane.
Dr Fionnuala Lundy
Institution: Oral Science Research Centre, Queen's University, Belfast
Amount: £18,957
Title: ‘The expression and functionality of antimicrobial peptides in the gingival crevice in type 1 diabetes’
Lay summary: Diabetic patients suffer an increased risk of many diseases, including periodontal (gum) disease in which the bone which supports the teeth is gradually destroyed leading to the teeth becoming loose and eventually being lost. Even in the early stages of periodontal disease, the gums become inflamed and bleed, making it difficult for diabetic patients to eat healthily (and maintain blood sugar control). Diabetic patients are three times more likely to be affected by periodontal disease than non-diabetics. We know that effective treatment of gum disease also improves the control of diabetes. If we are to tackle the problem of periodontal disease in diabetic patients, then we need to understand how the bacteria that cause periodontal disease are normally kept under control.
The cells in our gum tissues make molecules called antimicrobial peptides that defend against the invasion of bacteria that cause periodontal disease. In this project we will build upon our previous research on naturally occurring antimicrobial peptides in the mouth to determine if these peptides are present and if they work effectively in diabetics. Our study should enable better treatments to be specifically designed to treat periodontal disease in diabetic patients.
Professor Michael Edmonds
Institution: Diabetes Foot Clinic, King's College Hospital, London
Amount: £11,038 (part-funded)
Title: ‘Is Charcot osteoarthropathy a Cytokine-Driven Disease?’
Lay summary: Some people with diabetes and nerve damage can develop a devastating form of bone and joint disease known as the “Charcot foot” in which there is considerable bone destruction, caused by cells called osteoclasts. The cause of this bone destruction is not fully understood. We have recently shown that the activity of these osteoclasts is increased in patients with acute Charcot foot. One possible reason may be an increase in the cells in the blood, called special monocytes, from which these osteoclasts are derived. Special monocytes are increased in patients with Charcot foot. There are also substances in the blood which can affect the development of osteoclasts.
The aim of this study is to measure the level of these substances in patients with acute Charcot foot and also to assess whether any of them show a relationship with the increased number of the special monocytes. If we do find a relationship we need to be sure that it is related to the Charcot foot and therefore we will also carry out these measurements in a group of diabetic patients without Charcot foot, and in a group of healthy subjects. It is hoped that if we discover the factors that lead to increased number of special monocytes and thus increased osteoclastic activity, this will help the understanding of bone destruction and lead to new treatments for this devastating condition.