Abstract
The hypothesis that idiopathic diabetes is a result of insufficient secretion of insulin seemed to be confirmed by many earlier experimental studies carried out around the turn of the century. This viewpoint was based on the studies of von Mering and Minkowski1 who, in 1889, were the first to observe that removal of the pancreas causes diabetes in the dog. The discovery of insulin by Banting and Best2 in 1922 seemed to support this hypothesis, as the administration of pancreatic extracts could correct the metabolic abnormalities in diabetes. This was in keeping with the frequently observed atrophy of the pancreatic islets,3–7 the decrease of extractable insulin8–10 in the pancreases of juvenile diabetics, and the occurrence of interacinar fibrosis, insular fibrosis, and hyalinization in the pancreases of maturity-onset diabetics.11 Moreover, quantitative studies by various investigators indicated a relative increase of A cells in many diabetic pancreases associated with a concomitant decrease of B cells.7,12–14 On the other hand, in more recent studies,14ait was observed that in type II diabetes the mass of B, D, and PP cells was unchanged, while that of A cells was increased. The hyperplasia of A cells led to decreased B/A and D/A cell ratios. This discrepancy of observations, it was conjectured,14a may be due to the fact that in the latter studies more sensitive immunocytochemical techniques were used that permitted the detection of poorly granulated B cells and/or that the population of patients used in these various studies may have been different.
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References
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Volk, B.W., Wellmann, K.F. (1985). Pathogenetic Considerations of Type II Diabetes. In: Volk, B.W., Arquilla, E.R. (eds) The Diabetic Pancreas. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-0348-1_11
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DOI: https://doi.org/10.1007/978-1-4757-0348-1_11
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