Oral Presentation The Annual Scientific Meeting of the Australian Diabetes Society and the Australian Diabetes Educators Association 2013

Type 1 Diabetes from the human perspective (#139)

Olle Korsgren 1
  1. Uppsala University, Uppsala, Sweden

The mechanism(s) responsible for the destruction of the pancreatic beta-cells in humans remains unknown. At present our view on the etiology of TID originates to a large extent from information gained in two animal models, i.e. the NOD mouse and the BB rat. In both models a progressive T cell mediated destruction of the beta cells occurs. Unfortunately, the immunopathological findings in these small animal models of TID show limited similarities with the human disease. In human pancreatic specimens obtained at the onset of TID insulitis is discrete and heterogeneously distributed within the gland. Also, attempts to prevent disease progression with immunesuppression or immuneinterventions causes no or only transient preservation of beta cell function and do not halt the progression to clinically established TID. Hence, in humans there is limited support for T1D being primarily an autoimmune disease. Furthermore, available information demonstrates that affection of the exocrine pancreas in T1D is underappreciated. Autoantibodies to exocrine cells, exocrine pancreatic insufficiency and a substantial reduction in pancreatic volume are present already early after T1D diagnosis. In subjects with recent onset T1D focal or diffuse lesionsof acute pancreatitis, often centered around the pancreatic ducts, are frequently observed. Collectively available information in humans argues strongly that T1D is an inflammatory disease affecting the entire pancreas, but with its main clinical manifestations emanating from the loss of the insulin producing cells.