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Home > News & events > News > Research breakthrough shows insulin-producing cells can be regenerated
During the development of type 1, the immune system mistakenly attacks the insulin-producing beta cells in the pancreas. This stops people with the condition being able to make their own insulin and means that they require lifelong insulin replacement therapy.
Replacing the damaged beta cells either from external sources or triggering the regeneration of beta cells within the body could potentially reduce or eliminate the need for insulin injections in individuals with type 1 diabetes.
We know that islet transplantation and whole pancreas replacement using donor tissues or organs reduces or removes the need for injecting insulin in those with type 1. However, the limited availability of donors, along with the need for life-long immunosuppression, make this option unsuitable for the majority of people living with the condition.
This is why finding ways to regenerate the body’s lost beta cells is so important.
The research project, funded by JDRF and led by Professor Sam El-Osta from the Baker Heart and Diabetes Institute, investigated whether treatment with two drugs could regenerate insulin-producing cells in donor pancreases.
Using donor pancreases from a child and adult with type 1, and from a donor without type 1, the team demonstrated that pancreatic cells that don’t normally produce insulin – called ductal cells –could be made to behave like beta cells using two drugs known as EZH2 inhibitors (GSK 126 and Tazemetostat). Specifically, these newly generated beta-like cells were able to express genes that are associated with beta cells and, importantly, produce and secrete insulin.
The drug GSK126 is already FDA-approved for use in other diseases. The research project was the first time Tazemetostat has been used for this purpose.
These are incredibly exciting findings, as they suggest there is a pathway for people with type 1 to restore insulin production, potentially using cells from their own body. This method could remove the need for immunosuppressive treatments used with pancreas replacements and could address the issue of limited availability of donated islets needed for islet transplantation.
These therapies work in a different way to other therapies also being investigated which halt the immune system attack. These findings represent another avenue to tackle type 1 and enable everyone living with the condition to potentially achieve independence from round-the-clock insulin injections.
JDRF has been involved from an early stage of this research, with this breakthrough an extension of previous JDRF funded work also led by Professor El-Osta and his team.
Further work with pre-clinical models are now needed to take this research to the next stage. This is why we have already committed over £500,000 to extend this project.
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