ABSTRACT
Diabetes mellitus is a chronic disease defined by chronic hyperglycemia. Major progress was achieved in the 70’s when the distinction was made between type I and type II diabetes. Type I diabetes is defined as a disease state requiring the daily administration of insulin for metabolic control (insulin dependent diabetes mellitus, IDDM). Type II diabetes, which is also associated with hyperglycemia and glycosuria (but without spontaneous evolution to ketosis), is characterized by usual absence of requirement for insulin therapy (non-insulin dependent diabetes mellitus, NIDDM). In addition to these important clinical differences, type I and type II diabetes differ by their putative underlying mechanisms. The vast majority of cases of type I diabetes relate to an autoimmune pathogenesis according to which the β cells of islets of Langerhans, which produce insulin, are destroyed by autoreactive T cells (1). Type II diabetes, in most cases, is a genetically controlled, purely metabolic disease enhanced by additional factors such as obesity leading to insulin resistance that the patients cannot overcome, probably due to some yet undefined β-cell failure. Recent data have indicated that 5-15% of type II diabetes cases are, in fact, also autoimmune (slow type I or late autoimmune diabetes of the adult, LADA) (2,3).
