Exp Clin Endocrinol Diabetes 1988; 91(2): 161-170
DOI: 10.1055/s-0029-1210739
Original

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

The Endocrine Pancreas of BB/OK-Rats before and at Diagnosis of Hyperglycaemia

Silke Lucke, W. Besch, Christiane Kauert, H. J. Hahn
  • Central Institute of Diabetes “Gerhardt Katsch” (Director: OMR Prof. Dr. sc. med. H. Bibergeil), Karlsburg/GDR
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Publikationsverlauf

1987

Publikationsdatum:
16. Juli 2009 (online)

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Summary

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 β-cell volume density were visible. Despite of this great heterogeneity two types in the course of β-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 β-cell mass already more than 60 days before diagnosis of hyperglycaemia significantly reduced, occurrence of insulitis) whereas other animals show an acute form of β-cell destruction (still about 20 days before diagnosis of diabetes pancreatic insulin content and relative β-cell volume density in a normal range). Besides a drastical reduction of pancreatic insulin content at the time of diabetes diagnosis intense mono-nuclear infiltrations in the islets of Langerhans causing their destruction are demonstrable. As a result the residual β-cell volume is significantly reduced. Rats with a plasma glucose higher than 13 mmol/l at diagnosis do not have any demonstrable β-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 β-cells.

We conclude that prospective statements on the development of diabetes on the strength of analysis of residual β-cells and pancreatic insulin content are not possible at present. We suppose that there exist different processes of β-cell destruction which have to be investigated in further studies including immunological parameters.