Type I diabetes is probably due to the immune-mediated destruction of islet insulinsecreting β-cells. This chronic destructive process is associated with both cellular and humoral immune changes in the peripheral blood that can be detected months, even years, before the onset of clinical diabetes. Throughout this prediabetic period, metabolic changes, including altered glucose tolerance and reduced insulin secretion, deteriorate at variable rates toward full-blown diabetes. The ability to predict subsequent clinical diabetes in those nondiabetic individuals with immune and metabolic changes has led to attempts to prevent the disease onset by therapeutic intervention. A small fraction of individuals with immune changes develop clinical diabetes that does not require insulin treatment. The onset of diabetes in these cases is usually in adult life, and because their diabetes is, at least initially, not insulin-dependent, they appear clinically to have type II diabetes. Such patients probably have the same disease process as patients with type I diabetes in that they have similar human leukocyte antigen (HLA) genetic susceptibility as well as autoantibodies to islet antigens. It is proposed that non-insulin-dependent diabetic patients who have markers that characterize individuals at risk of type I diabetes may be suitable candidates for those same therapeutic strategies that seek to prevent progression to insulin-dependence or even to reestablish normal glucose tolerance.

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