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Funded Research

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  • 2020
    Pump Priming

    5HT2C receptor agonism to lower blood glucose. Proof of concept in humans

    Recipient:
    Dr Rajna Golubic
    Institution:
    University of Cambridge
    City:
    Cambridge
    Amount:
    £20,000
    Description: 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 potenti...
    Description: 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

    Recipient:
    Professor Gwyn Gould
    Institution:
    University of Strathclyde
    City:
    Glasgow
    Amount:
    £19,926
    Description: 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 numb...
    Description: 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

    Recipient:
    Professor Calum Sutherland
    Institution:
    University of Dundee
    City:
    Dundee
    Amount:
    £19,693
    Description: 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 ...
    Description: 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?

    Recipient:
    Professor Kathleen Gillespie
    Institution:
    University of Bristol
    City:
    Bristol
    Amount:
    £18,000
    Description: 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 d...
    Description: 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?

    Recipient:
    Dr Mark Russell
    Institution:
    University of Exeter
    City:
    Exeter
    Amount:
    £20,000
    Description: 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...
    Description: 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 stateof-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.

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