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Abstract

The maintenance of appropriate plasma insulin levels is the result of two major mechanisms, namely minute-to-minute regulation of the insulin release from individual B-cells and long-term adaptation of the total B-cell mass to the peripheral demand for insulin. Diabetes mellitus is characterized by an inadequate supply of insulin resulting in severe hyperglycemia and disastrous vascular complications. In the case of insulin-dependent diabetes mellitus (IDDM), this inadequacy clearly reflects B-cell destruction, most probably caused by autoimmune aggression [57, 45]. In the case of non-insulin-dependent diabetes mellitus (NIDDM), the pathogenesis is less obvious, although there is evidence to suggest that in patients with NIDDM an increased peripheral insulin requirement is combined with a genetic deficiency in the ability of the B-cell to replicate [24, 68–70, 85] and a reduced insulin response to glucose [44]. It has furthermore been proposed that B-cell regeneration may also be of some significance in the course of IDDM, since in the early stages of the disease some patients exhibit both morphological and functional signs of a returning insulin production (“the honeymoon period”) possibly reflecting an effort of the reduced B-cell mass to meet the insulin demand.

The work by the authors included in this review was supported by the Swedish Medical Research Councl (12X-109, 17X-07501, 12P-6947), the Swedish Diabetes Association, the Nordic Insulin Fund, the Novo Company, the Expressen Prenatal Research Foundation, the Edla Johansson Fund, the Åke Wiberg Fund, the Ernfors Diabetes Foundation, the Juvenile Diabetes Foundation International, and the Kroc Foundation.

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Hellerström, C., Swenne, I., Andersson, A. (1988). Islet Cell Replication and Diabetes. 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_9

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