Influence of the mutation "diabetes" on insulin release and islet morphology in mice of different genetic backgrounds
(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)
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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.
- author
- Boquist, L. ; Hellman, B. ; Lernmark, Å LU and Täljedal, I. B.
- publishing date
- 1974-07-01
- 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
-
- pmid:4135113
- scopus:0016204314
- 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
- 2024-03-13 08:19:00
@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}}, }