Autoimmunity Markers in Patients with Type 2 Diabetes

Diabetes is not a single disease entity. Conducted over the past decades, research and clinical enabled the understanding of this heterogeneity. In 1997, it announced the etiological division of diabetes, which distinguishes two main forms: type 1 and type 2. In the pathogenesis of both forms genetic and environmental factors play the role. Type 1 develops as a result of autoimmune destruction of pancreatic islet B cells. This represents approximately 10% of all cases of the disease. 

Type 1 diabetes is associated with the presence of autoantibodies against antigens of B cells and carriers of certain alleles of the major histocompatibility passed to it more often than the general population.

Type 2 is the more common form, representing about 90% of all cases of the disease in the developed regions of the world civilization. It is characterized by the coexistence of insulin deficiency and the peripheral effects of the hormone. Immunological markers do not appear, and the genetic basis has no connection with the HLA system.

In addition, there is rising incidence of type 2 diabetes in children and adolescents. In the end, the last two decades have produced important findings about monogenic forms of diabetes, revealing mainly in the developmental age and young adults. These findings have proved that diabetes has much more diverse etiology, than recently thought.