Type 1 diabetes mellitus (DM) arises from selective immunologically mediated destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans with consequent insulin deficiency.1,2 This occurs in genetically susceptible individuals and is a cellular-mediated process, presumably a specific reaction to 1 or more beta cell proteins (autoantigens), although probably initiated by some environmental factors. There is consequent progressive impairment of beta cell function and decline in beta cell mass.
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