Scientists have discovered why type 1 diabetes is particularly severe in young children

The new work, published in the journal Science Advances, provides the clearest explanation to date for why the early form of the disease is harder to control and requires higher doses of insulin.

Type 1 diabetes is an autoimmune disease in which the immune system destroys insulin-producing cells in the pancreas. In children, usually under the age of seven, the disease develops more rapidly, is more likely to lead to emergencies and is harder to manage than in patients diagnosed at an older age.

Until now, researchers have had few tools to study the early development of insulin-producing cells in detail. These cells are gathered in small clusters in the pancreas. In young children, these clusters are still forming, are small in size and contain only a few insulin-producing beta cells.

The team, led by Professor Sarah Richardson from the University of Exeter, used advanced tissue analysis techniques to look at these tiny structures with unprecedented precision. The scientists examined rare pancreas samples from more than 250 people of different ages - both with and without type 1 diabetes - and tracked how these clusters change with age and under the influence of the immune system.

The results confirmed: young children without diabetes have many small clusters of insulin-producing cells. As they grow older, they increase in size and mature, especially rapidly in the first years of life.

For the first time, it has been shown that in people with type 1 diabetes, these small clusters almost completely disappear - they are destroyed by the immune system. Some patients are left with a few large structures that allow them to maintain a small amount of their own insulin production, but those diagnosed at an early age have virtually no such large accumulations.

Taken together, the evidence suggests that it is the numerous small clusters of beta cells in young children that are most vulnerable to autoimmune attack. Their rapid destruction prevents them from maturing into larger, more stable structures, leaving very few cells capable of producing insulin. This explains why, when the disease makes its early debut, children retain little or no of their own insulin production and need particularly careful management of the disease.

The study highlights the key role of these "small" clusters in normal pancreatic development and paves the way for new therapies aimed at protecting beta cells in children. If these structures can be preserved and allowed to mature into large clusters, their vulnerability to immune attack could be reduced. The work also strengthens the case for early screening of type 1 diabetes, especially in young children, to detect the disease in its earliest stages - before critical cells are lost.

"These tiny clusters of beta cells, previously left in the shadows, provide major clues to understanding type 1 diabetes. A new look at them has the potential to change approaches to screening, treatment and even prevention of the disease," emphasises Professor Sarah Richardson. Protecting small clusters of beta cells at an early stage could be the key to halting the development of type 1 diabetes before it becomes clinically apparent, she says.