Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

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

Boquist, L. ; Hellman, B. ; Lernmark, Å LU orcid and Täljedal, I. B. (1974) In Journal of Cell Biology 62(1). p.77-89
Abstract


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... (More)


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.

(Less)
Please use this url to cite or link to this publication:
author
; ; and
publishing date
type
Contribution to journal
publication status
published
in
Journal of Cell Biology
volume
62
issue
1
pages
77 - 89
publisher
Rockefeller University Press
external identifiers
  • scopus:0016204314
  • pmid:4135113
ISSN
0021-9525
DOI
10.1083/jcb.62.1.77
language
English
LU publication?
no
id
a74701e5-0eae-49bc-8bda-9471912ac5ee
date added to LUP
2019-09-18 12:17:28
date last changed
2025-10-14 11:15:59
@article{a74701e5-0eae-49bc-8bda-9471912ac5ee,
  abstract     = {{<p><br>
                            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<br>
                            <sup>2J</sup><br>
                            , 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<br>
                            <sup>2J</sup><br>
                            /db<br>
                            <sup>2J</sup><br>
                             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<br>
                            <sup>2J</sup><br>
                            /db<br>
                            <sup>2J</sup><br>
                             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.</p>}},
  author       = {{Boquist, L. and Hellman, B. and Lernmark, Å and Täljedal, I. B.}},
  issn         = {{0021-9525}},
  language     = {{eng}},
  month        = {{07}},
  number       = {{1}},
  pages        = {{77--89}},
  publisher    = {{Rockefeller University Press}},
  series       = {{Journal of Cell Biology}},
  title        = {{Influence of the mutation "diabetes" on insulin release and islet morphology in mice of different genetic backgrounds}},
  url          = {{http://dx.doi.org/10.1083/jcb.62.1.77}},
  doi          = {{10.1083/jcb.62.1.77}},
  volume       = {{62}},
  year         = {{1974}},
}