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Controlling Blood Glucose Levels in Mice: A New Type 1 Diabetes Development
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Controlling Blood Glucose Levels in Mice: A New Type 1 Diabetes Development

Controlling Blood Glucose Levels in Mice: A New Type 1 Diabetes Development
News

Controlling Blood Glucose Levels in Mice: A New Type 1 Diabetes Development

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Researchers in Belgium have successfully generated insulin-producing beta cells from other pancreatic cells in mice with type 1 diabetes. The mice were then able to control their own glucose levels without additional insulin.

The study, part-funded by JDRF, the type 1 diabetes charity, was published today in Nature Biotechnology.

In those living with the condition, the immune system attacks the beta cells of the pancreas, leaving the person unable to produce insulin. This means they cannot control their own blood glucose, and must rely on insulin injections to stay alive.

However, the other pancreatic cells remain functional, and reprogramming these to produce insulin is a potential pathway to treating the condition.

The researchers simulated type 1 diabetes in the mice and after five weeks, some of these mice received a course of proteins (epidermal growth factor and ciliary neurotrophic factor) that have been known to stimulate beta cell growth in the lab.

The treated mice subsequently began producing insulin, and their blood glucose levels fell to match those of mice with functioning beta cells. The other mice continued to experience hyperglycaemia (high blood glucose levels).

By tracing the genetic origin of the newly grown beta cells, the researchers found that they were mostly derived from another type of pancreatic cell, called acinar cells. These normally help the pancreas secrete digestive juices, and are not involved in insulin production.

Dr. Harry Heimberg, Principle Investigator from Diabetes Research Centre at the University of Brussels, said: “Acinar cells can be reprogrammed to beta-like cells in the laboratory. Several characteristics make acinar cells ideal candidates for reprogramming to beta cells in the pancreas as well: they are the most abundant cell type, their microenvironment is identical to that of beta cells and they are not affected by diabetes."

This study provides hope for those living with type 1 diabetes, but more research will be necessary to see if the findings can help those living with the condition, as it is likely that the immune system would still attack any newly-formed beta cells.

Dr Heimberg added: "We hope that our model will contribute to the development of a robust and safe strategy for beta cell therapy in diabetes."

Karen Addington, Chief Executive of JDRF, said: “The results from this study are interesting, and certainly appear deserving of further exploration. Type 1 diabetes is a challenging and complex condition. But it will one day be cured. It's just a matter of time, money and excellent research."

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