In the mid 1960s, the Belgian histopathologist Gepts  first described lymphocytes infiltrating the islets of children who died within a few days of developing diabetes. In 1974, Nerup et al.  found an association between childhood diabetes and the immune response or HLA genes on the short arm of chromosome 6. That same year, Bottazzo et al.  reported the presence of antibodies to the islet cells in blood samples from people with insulin-dependent diabetes.
Together, these observations prompted a radical revision in the understanding of diabetes. The prevailing model of diabetes as a single disorder that could present either in childhood (juvenile onset) or later in life (adult onset) was replaced by a classification that clearly distinguished type-2 diabetes (then almost exclusively a disorder of later adulthood) from type-1 diabetes. Type 1 became known as autoimmune diabetes, caused by a dysregulated immune system that attacks, and ultimately destroys, the p cells.
The past three decades have seen an exponential rise in the incidence of diabetes - most noticeably of type 2, owing to the greater numbers involved, but also of type-1 diabetes. While type-2 diabetes is widely understood to be linked to obesity and the insulin resistance it causes, the rise in type 1 has not been satisfactorily explained.
Was this article helpful?