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Abstract

Nearly 100 years ago, the pathogenesis of diabetes mellitus was linked to the pancreas [1]. Later, at the beginning of this century, some investigators reported islet lesions in diabetic individuals which included fibrosis, hyalinosis, hydropic degeneration, atrophy and inflammatory reactions [2]. However, the islets of Langerhans were yet to be linked to the production of insulin and the etiology and pathogenesis of diabetes remained unclear. Insulin was extracted from the pancreas in 1921 and proved to ameliorate most of the diabetic symptoms [3]. It soon became clear, however, that insulin was not a cure for diabetes. In 1965, Gepts [4] reported that the major morphologic alteration in the pancreas at the onset of IDDM was a disruption of the architecture of the islets of Langerhans and a loss of B-cells. The number of B-cells was reduced to less than 10% of normal values and in 68% of the pancreases examined, the islets were infiltrated by mononuclear cells. Islet inflammation, insulitis, was therefore suggested to be of pathogenetic importance [4–7]. Infiltration of the islets of Langerhans has also been associated with experimental diabetes induced by immunization with insulin [8–9], by multiple injections of low-dose streptozotocin [10], or following infection with diabetogenic viruses [11,12].

The work in the authors’ laboratory has been supported by the foundation Nordisk Insulinlaboratorium, The National Institutes of Health (grants DK26190, DK33873), and the Juvenile Diabetes Foundation. Steinunn Baekkeskov is supported by a Juvenile Diabetes Foundation Career Development Award.

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Lernmark, Ä., Markholst, H., Baekkeskov, S. (1988). Circulating Signs of Autoimmune Islet Disease. In: Lefèbvre, P.J., Pipeleers, D.G. (eds) The Pathology of the Endocrine Pancreas in Diabetes. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-72691-0_4

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