Scientists have long tried to understand why, in type 1 diabetes, the immune system suddenly begins destroying the pancreas cells responsible for producing insulin. Many theories exist, but no definitive explanation has been found so far. A new study from the University of Florida Diabetes Institute adds an important piece to this complex puzzle.

The research was published in the journal Diabetes.

The scientists discovered that the earliest targets of the immune system are the smallest clusters of insulin-producing beta cells, as well as solitary beta cells scattered throughout the pancreatic tissue. This appears to occur even before the first symptoms develop. According to the authors, the loss of these tiny cell groups may signal the next phase of the disease, when the immune system begins attacking the larger and more vital beta-cell clusters — the islets of Langerhans.

Lead author Clive Wasserfall says the sequence of cellular destruction surprised the researchers, and they can only hypothesize why the smallest structures die first. If the larger islets of Langerhans can be protected, it may be possible to slow the onset of the disease. Understanding how type 1 diabetes develops helps shape new strategies for combating it, even though a full cure remains distant. This discovery may eventually allow physicians to detect the disease at earlier stages and intervene in time to slow its progression.

Interestingly, the small beta-cell clusters have rarely been the focus of scientific research. Traditionally, studies have concentrated on the islets of Langerhans. However, analysis of tissue samples from the world’s largest pancreas biobank for diabetes research showed that the smaller cell groups are the first to disappear, while the larger islets remain nearly intact for some time. This may also explain why the disease progresses so rapidly in young children, while adults sometimes retain some natural insulin production for a longer period.