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Keeping beta cells beating

Project summary

In diabetes, insulin-making beta cells in pancreas have either been destroyed or don’t work properly. Dr Liu is researching a molecule called miR-33 to see if blocking it could help beta cells to work better. This could lead to new treatments for type 2 diabetes and improvement transplants of beta cells for people living with type 1.

Background to research

Type 1 diabetes occurs when the beta cells in the pancreas that make insulin are destroyed. In type 2 diabetes the same cells don’t release enough insulin or the insulin doesn’t work as well.   

Dr Liu and her team have found an interesting molecule in beta cells known as miR-33. This molecule acts to reduce the number of beta cells in the pancreas and the amount of insulin that’s released. She’s also shown you can improve the function of beta cells if you stop miR-33 from working. 

Some people with type 1 diabetes who have severe hypos and no awareness of them are eligible for transplants of donor beta cells, called islet transplants. But one of the problems with islet transplants is that a lot of the beta cells fail after transplant. For people with type 2 diabetes, treatments that make better cells work better would also be revolutionary.  

Research aims

Dr Liu aims to find out more about the effects of blocking miR-33 and how this can help beta cells to better control blood sugar levels. To do this, Dr Liu will use mice that have their miR-33 molecule switched off in their beta cells. One way of doing this is by using the drug fluoxetine, which is the active part of an antidepressant treatment known as Prozac.  

She’s also going to see if this using fluoxetine could make islet transplants more successful – helping donors' cells to survive and make more insulin – by treating mice with type 1 diabetes. 

Potential benefit to people with diabetes

Dr Liu’s research will help us understand how miR-33 affects beta cells and insulin release to control blood sugar levels. 

In the future, this may lead to therapies that stop miR-33 in beta cells to prevent or treat type 2 diabetes. It may also give us a way of making islet transplants more effective so that more people with type 1 diabetes can benefit from this exciting treatment. 

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