Lucke S, Besch W, Kauert C, Hahn H J
Central Institute of Diabetes Gerhardt Katsch, Karlsburg/GDR.
Exp Clin Endocrinol. 1988 May;91(2):161-70. doi: 10.1055/s-0029-1210739.
From 148 BB-rats 76 animals (51.4%) developed hyperglycaemia within 55th to 178th day of life. Already before diagnosis of diabetes a great variety in pancreatic insulin content and morphometrically determined relative beta-cell volume density were visible. Despite of this great heterogeneity two types in the course of beta-cell destruction could be observed. Verified by individual retrospective analysis one part of the rats is characterized by a more chronical course of diabetes development (pancreatic insulin content and beta-cell mass already more than 60 days before diagnosis of hyperglycaemia significantly reduced, occurrence of insulitis) whereas other animals show an acute form of beta-cell destruction (still about 20 days before diagnosis of diabetes pancreatic insulin content and relative beta-cell volume density in a normal range). Besides a drastical reduction of pancreatic insulin content at the time of diabetes diagnosis intense mononuclear infiltrations in the islets of Langerhans causing their destruction are demonstrable. As a result the residual beta-cell volume is significantly reduced. Rats with a plasma glucose higher than 13 mmol/l at diagnosis do not have any demonstrable beta-cells and an insulin content on the lowest detection limit of the method. In animals with a more mild hyperglycaemia (plasma glucose 8.3 to 13 mmol/l) there are rats with and the other ones without immunohistochemically detectable beta-cells. We conclude that prospective statements on the development of diabetes on the strength of analysis of residual beta-cells and pancreatic insulin content are not possible at present. We suppose that there exist different processes of beta-cell destruction which have to be investigated in further studies including immunological parameters.
