Funded Research
Our Research Funding
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.
2020
Pump Priming
5HT2C receptor agonism to lower blood glucose. Proof of concept in humans
- Description - click to read
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Despite many advances in the treatment of diabetes, relatively few people are able to achieve optimal glucose levels to reduce risk of complications. In our proposed study, we will examine the potential for a new approach to lowering blood glucose. Lorcaserin is a drug currently used for weight loss and acts on brain pathways that regulate appetite. In mice, we found that in addition to altering body weight, lorcaserin lowers blood glucose by acting on brain pathways to regulate the liver and perhaps pancreas. This glucose lowering effect of lorcaserin has not been studied in humans yet and we aim to do so. If ultimately proven effective, lorcaserin or similar treatments could potentially be used in diabetes (including those treated with insulin as an “add on” treatment) to improve glucose levels and reduce the risk of complications and substantial healthcare costs associated with this.
2020
Pump Priming
A yeast-based screen for novel regulators of GLUT4 trafficking
- Description - click here to read
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It’s insulin that mainly regulates glucose levels in our blood. It gets glucose into fat and muscle cells where the glucose is stored until blood sugar levels fall. It does this by increasing the number of specialised ‘glucose transporter’ proteins on the cell surface. It moves these glucose transporters from a storage depot inside the cell to the cell surface. This process doesn’t work so well if you have Type 2 diabetes. Not enough is known about what controls this movement of transporters - and this is holding back the development of an effective therapy. Our group has used brewer's yeast as tool to identify a new control mechanism used by fat and muscle to regulate glucose transporters. We will use this to find out new details about how insulin works.
2020
Pump Priming
An investigation of insulin receptor biology to improve our understanding of the development of insulin resistance and Type 2 diabetes
- Description - click here to read
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Insulin does not work properly in people with Type 2 diabetes (T2D). This ‘insulin resistance’ occurs even before T2D diagnosis. Insulin is detected by a receptor on the cell surface. The receptor is like a lock, and insulin is the key, that triggers the cell to take up glucose and store it properly. We want to understand why this lock and key system goes wrong, leading to T2D. We have found that the receptor gets cut in two by an enzyme called BACE1 (which is high in people with T2D). Therefore, BACE1 inhibitors could be used to help insulin work better. However other work suggests that splitting the receptor may be a normal part of how insulin works. We propose to change BACE1 in liver and brain cells and measure insulin action. This information will establish whether BACE1 inhibitors would help, or cause problems for, people with T2D.
2020
Pump Priming
Does a leaky gut increase risk of diabetes in children with Down’s syndrome?
- Description - click here to read
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Children with Down's syndrome who have one extra copy of chromosome 21 are four times more likely to develop type 1 diabetes than children from the general population. In addition, when they do develop the condition, it appears to happen earlier in life. Like individuals with type 1 diabetes, children with Down's syndrome are also at increased risk of gut and thyroid autoimmunity. We have recruited 99 babies to date with Down's syndrome to investigate early life experiences in detail. We have also collected a wide bank of samples for analysis. In this application, we ask for funds to allow us to test whether a leaky gut predicts onset of diabetes in children with Down's syndrome.
2020
Pump Priming
Is mitochondrial STAT3 a novel regulator of insulin secretion?
- Description - click here to read
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STAT3 is a molecule which controls the levels of specific genes in cells. However, recently, a form of STAT3 was discovered which has a different function - modifying energy production by changing the activity of the cell’s power generators known as mitochondria. This may be important for beta-cells of the pancreas, since increases in energy production are essential for their ability to produce insulin (a hormone important for blood glucose control). In this project we will use genetic-engineering to create beta-cells which have one of two different versions of STAT3: either a variant which prefers to move to the mitochondria or one which is unable to. We will then use state of-the-art technology to assess whether energy generation and insulin production changes in these cells. If successful, data generated from this study may help in the design of novel drugs which could increase insulin production in people with diabetes.
2020
Pump Priming
Novel genetic insights into autoimmune diabetes
- Description - click here to read
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We do not fully understand how destruction (autoimmunity) of the insulin-producing cells in the pancreas develops in type 1 diabetes (T1D). A condition which is very similar to T1D, and much easier to study, is monogenic autoimmune diabetes which is caused by a single letter change (a mutation) in an individual’s DNA. Studying patients with monogenic diabetes will provide new insights into how insulin-producing cells are destroyed which will increase understanding of T1D. We will use a powerful genetic technique (genome sequencing) to find the single letter change that is causing destruction of the insulin-producing cells in individuals with suspected monogenic autoimmune diabetes providing a genetic diagnosis to the families. Furthermore, these findings will identify new biological pathways which are responsible for the development of autoimmunity that will have important implications for patients with more common type 1 diabetes.
2020
The Professor David Matthews Non-Clinical Fellowship
Identifying islet antigen specific lymphocytes by recruitment to intradermally injected autoantigens, using single cell RNA sequencing: a route to novel cell based therapies and immune monitoring
- Description - click to read
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Immunotherapy in type 1 diabetes aims to reduce the body's immune attack on the insulin-producing beta cells. To develop these treatments, it is important to be able to identify and monitor the white blood cells that cause the damage. We cannot study these cells safely in the pancreas and numbers in the blood are very low. However, I have observed that after injecting molecules derived from the beta cells into the skin, I can detect white blood cells multiplying in skin. I have also been able to detect cells multiplying in lymph glands that drain the skin using ultrasound guided needle sampling. These are likely to be cells from the pancreas attracted to the skin by the injection of pancreas derived protein. I will study these cells using state-of-the-art single cell analysis technology and use this information to develop highly targeted treatments for the immune response in type 1 diabetes.
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