Reactivating dormant beta cells can help treat type 1 diabetes

Children who are diagnosed with diabetes before the age of seven develop a more aggressive form of the disease than that seen in teenagers, new research suggests.

The study provides the first clear evidence of the impact being diagnosed with type 1 diabetes has on children before they reach primary school age.

A condition known as insulitis, representing an inflammatory process, kills off nearly all the insulin-producing beta cells in the pancreas of the young children.

Researchers found the progression of the disease is radically different in those diagnosed as teenagers or beyond.

They retain unexpectedly large numbers of beta cells at diagnosis - although they are no longer working as they should.

The discovery was made by a team led by the University of Exeter Medical School who said their work could lead to new treatments.

They worked with the University of Oslo and the network of Pancreatic Organ Donors (nPOD) to analyse the largest collection of biobanked pancreas samples from people with type 1 diabetes.

Professor Noel Morgan said: "This is incredibly exciting, and could open the doors to new treatments for young people who develop diabetes.

"It was previously thought that teenagers with type 1 diabetes had lost around 90% of their beta cells but, by looking in their pancreas, we have discovered that this is not true.

"In fact, those diagnosed in their teens still have many beta cells left - this suggests that the cells are dormant, but not dead.

"If we can find a way to reactivate these cells so that they resume insulin release, we may be able to slow or even reverse progression of this terrible disease."

In the UK alone, around 30,000 young people have type 1 diabetes, and diagnoses among the younger age group are escalating fast.

A child diagnosed with the disease at the age of five faces up to 19,000 insulin injections and 50,000 finger-prick blood tests before they reach adulthood.

The team's discovery also has important implications for this younger group - for example, most trials have focussed mainly on halting the immune attack in older patients, where the team finds that insulitis may be less severe.

In future, it will be important to assess whether younger children might benefit most from such approaches, as they have the more aggressive disease.

The team analysed a subset of human samples from people with type 1 diabetes within the Exeter Archival Diabetes Biobank.

They then checked and extended their results against larger databases of samples from America and Europe, which confirmed their results.

Co-author Dr Sarah Richardson said: "For trials to be effective, we have to understand the underlying causes of the disease.

"Until now, most research into the onset of type 1 diabetes has been carried out in animal models. While that's extremely valuable, there are clear differences in human pathology.

"Here in Exeter, we now have this incredible resource of a unique biobank of human samples from people with type 1 diabetes, which means we're able to see what's really going on in the human body.

"We're working with partners across the world to make major advances in this research area. Our next step is to investigate why diabetes progresses differently in younger and older children, with a view to understanding how we could treat both groups more effectively."

The study, funded by the European Union and the type 1 diabetes charity JDRF, is published online in the journal Diabetes.

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