Pathophysiology of type 1 diabetes

Type 1 diabetes mellitus (T1DM) is characterized by defects in beta-cell function that eventually result in absolute insulin deficiency, requiring insulin replacement therapies to ensure survival and limit the complications of hyperglycemia. Type 1A or autoimmune diabetes, which accounts for 85% to 90% of T1DM, is characterized by the presence of autoantibodies to several islet cell molecules, including insulin, GAD, and IA-2, as well as by infiltration of the islets and destruction of beta cells by mononuclear cells (insulitis). Although the presence of insulitis requires a tissue specimen for diagnosis, autoantibodies on the other hand can be measured from serum and are detectable years prior to the onset of hyperglycemia. Along with genetic screening and assessment of stimulated insulin secretion, autoantibodies can also be used to predict the development of T1DM in at-risk populations.