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Abstract

Studies carried out over the past three decades in animal models and in patients suggest that Type 1 diabetes mellitus is an autoimmune disease. Elsewhere, in Chapter V, this work is reviewed and current concepts of disease pathogenesis are discussed. These studies indicate that the Type 1 diabetes is due to the T cell mediated destruction of the beta cells in the islets of Langerhans. The risk of diabetes in the general population in North America is approximately 12.5/100,000, although this number has been increasing.1 The risk of Type 1 diabetes is higher among families with another relative with Type 1 diabetes. The genetic locus most highly linked to the disease is the major histocompatibility locus (MHC), and over 90% of Caucasian individuals express either HLA DR3 and/or DR.2 Prediction of future diabetes, however, is not possible on a genetic basis alone. For example, the concordance rate for identical twins is < 50%, indicating that either environmental or developmental events (such as T cell development) affect the progression of diabetes.

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Thomas-Geevarghese, A., Herold, K.C. (2004). Diabetes Prevention. In: Poretsky, L. (eds) Principles of Diabetes Mellitus. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-6260-0_40

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