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Åke Lernmark

Principal investigator

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Influence of the mutation "diabetes" on insulin release and islet morphology in mice of different genetic backgrounds

Author

  • L. Boquist
  • B. Hellman
  • Å Lernmark
  • I. B. Täljedal

Summary, in English


Mice, 7-8-mo old, of the C57BL/KsJ-db strain and homozygotic for the mutant gene db, exhibited marked hyperglycemia and moderately elevated serum insulin levels. Light and electron microscopy provided evidence of a slightly decreased proportion of β cells in the pancreatic islets, irregular islet architecture with intraislet ducts, and degenerative as well as hypertrophic changes in the individual β cells. As a rule, islets microdissected from these mice did not release insulin in response to glucose, theophylline, iodoacetamide, or chloromercuribenzene-p-sul-phonic acid. The absence of secretory responses was not simply due to lack of insulin. Although the islet content of insulin was decreased in C57BL/KsJ-db/db mice, the remaining amount was severalfold larger than that released from stimulated islets of normal controls. Another mutation, db
2J
, an allele of db with identical phenotypic expressions in the C57BL/KsJ strain, was studied on the genetic background C57BL/6J. In contrast to the severely diabetic C57BL/KsJ-db/db animals, the C57BL/6J-db
2J
/db
2J
mice were characterized by highly elevated serum insulin levels and only moderate hyperglycemia. Their endocrine pancreas was enlarged and showed an increased proportion of β cells. Like the islets of normal mice, those of C57BL/6J-db
2J
/db
2J
mice responded to glucose and chloromercuribenzene-p-sulphonic acid, the glucose-induced responses being potentiated by theophylline or iodoacetamide. C57BL/KsJ-db/db mice should provide a valuable model for studying defects in insulin secretion in relation to diabetes mellitus. Mice of the C57BL/6J strain offer a control material that may help to elucidate the dependence of the insulin secretory defect on the background genome.

Publishing year

1974-07-01

Language

English

Pages

77-89

Publication/Series

Journal of Cell Biology

Volume

62

Issue

1

Document type

Journal article

Publisher

Rockefeller University Press

Status

Published

ISBN/ISSN/Other

  • ISSN: 0021-9525