Horm Metab Res 1980; 12(8): 349-353
DOI: 10.1055/s-2007-996291

© Georg Thieme Verlag, Stuttgart · New York

Insulin Secretion in Maturity-Onset-Diabetes Function of Isolated Islets

D. Lohmann1 , H. Jahr3 , H.-J. Verlohren1 , S. Schmidt3 , W. Heilmann1 , H. Zühlke3 , W. Hartig2 , H. Mättig2
  • 1Stadtkrankenhaus Leipzig, German Democratic Republic
  • 2Bezirkskrankenhaus Leipzig, German Democratic Republic
  • 3Zentralinstitut für Diabetes, Karlsburg, German Democratic Republic
Investigations carried out as part of the “Forschungsprojekt Diabetes mellitus und Fettstoffwechselstörungen” sponsored by the Ministry of Health of the German Democratic Republic.
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Publication History



Publication Date:
14 March 2008 (online)


An impaired insulin response to glucose is a characteristic finding in maturity onset diabetes (MOD). To clarify whether the decreased insulin response in vivo is related to a primary defect of the β-cells, isolated islets of MOD - obtained by intraoperative biopsy - were examined for their insulin content, biosynthesis and release. The in vitro experiments showed that despite a missing or significantly reduced insulin response in vivo the isolated β-cells of the same patients had a normal insulin content, a normal or even high biosynthesis, and insulin release could be induced by glucose. These results suggest that the primary defect in MOD cannot be related to an intrinsic failure of the β-cells to respond to glucose; extrapancreatic factors seem to influence their reaction to glucose. These factors may be of a higher level in those patients or the reaction of the β-cells is more inhibited by the same concentrations in diabetic patients.