Insulin-Dependent Diabetes Mellitus: Islet Changes in Relation to Etiology and Pathogenesis

Endocr Pathol. Winter 1997;8(4):273-282. doi: 10.1007/BF02739929.

Abstract

Type and type II diabetes are the most common types of diabetes. The ratio of type I to type II diabetes is about 1:9. Type I diabetes is caused by absolute insulin deficiency and is therefore referred to as insulin-dependent diabetes. The disease becomes manifest clinically in childhood or adolescence ("juvenile diabetes"), though onset in adulthood is increasingly being observed. Morphologically a subtotal (>80%) to total loss of B-cells in the pancreatic islets occurs. Lymphocytic insulitis, which disappears after the B-cells have been totally destroyed, is pathogneumonic of type I diabetes. This insulitis is an expression of an autoimmune event that is triggered by a multitude of factors. An important factor appears to be a genetic predisposition (human leukocyte antigen [HLA] DR3/DR4/DQ8) in connection with as-yet-unknown environmental factors (e.g., viruses). Autoantibodies, such as islet cell cytoplasmic antibodies (ICA). insulin autoantibodies (IAA) and/or autoantibodies to the gamma-aminobutyric acid (GABA)-synthesizing enzyme glutamic acid carboxylase (GAD), are already detectable in a prediabetic phase, though it is not possible to predict the time of clinical onset. The course of the disease is dependent on age. Young children require insulin therapy sooner than juveniles or adults.