Beta cell apoptosis is responsible for the development of IDDM in the multiple low-dose streptozotocin model

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Show simple item record O'Brien, B Harmon, BV Cameron, DP Allan, DJ 2012-02-10T06:09:18Z 1996-01
dc.identifier.citation Journal Of Pathology, 1996, 178 pp. 176 - 181
dc.identifier.issn 0022-3417
dc.identifier.other C1UNSUBMIT en_US
dc.description.abstract Although insulin-dependent diabetes mellitus (IDDM) results from irreversible loss of beta cells, the mode of cell death responsible for this loss has not previously been categorized. In this study, the multiple low-dose streptozotocin (stz) model (intraperitoneal injection of stz at a concentration of 40 mglkg body weight per day for five consecutive days) was used to investigate beta-cell death during the development of IDDM in male C57B116 mice. Apoptotic cells were evident by light microscopy within the islets of Langerhans of treated animals from day 2 (the day of the second stz injection) until day 17. Immunohistochemical localization of insulin to the dying cells confirmed the beta-cell origin of the apoptosis. Two peaks in the incidence of beta-cell apoptosis occurred: the first at day 5, which corresponded to an increase in blood glucose concentration, and the second at day 11, when lymphocytic infiltration of the islets (insulitis) was maximal. Insulitis did not begin until day 9, by which time treated animals had developed overt diabetes as revealed by blood glucose and pancreatic immunoreactive insulin (IRI) measurements. Beta-cell apoptosis preceded the appearance of T-cells in the islets and continued throughout the period of insulitis. Thus, whether induced by stz or a subsequent immune response, apoptosis is the mode of cell death responsible for beta-cell loss in the multiple low-dose stz model of IDDM.
dc.format Esha Dutt
dc.publisher Wiley
dc.title Beta cell apoptosis is responsible for the development of IDDM in the multiple low-dose streptozotocin model
dc.type Journal Article
dc.description.version Published
dc.parent Journal Of Pathology
dc.journal.volume 178
dc.journal.number en_US
dc.publocation UK en_US
dc.identifier.startpage 176 en_US
dc.identifier.endpage 181 en_US SCI.Medical and Molecular Biosciences en_US
dc.conference Verified OK en_US
dc.for 1103 Clinical Sciences
dc.personcode 030027
dc.percentage 100 en_US Clinical Sciences en_US
dc.classification.type FOR-08 en_US
dc.edition en_US
dc.custom en_US en_US
dc.location.activity en_US
dc.description.keywords apoptosis
dc.description.keywords streptozotocin
dc.description.keywords IDDM
dc.description.keywords mouse
pubs.embargo.period Not known
pubs.organisational-group /University of Technology Sydney
pubs.organisational-group /University of Technology Sydney/Faculty of Science
pubs.organisational-group /University of Technology Sydney/Strength - Health Technologies
utslib.copyright.status Closed Access 2015-04-15 12:17:09.805752+10
pubs.consider-herdc false
utslib.collection.history School of Medical and Molecular Sciences (ID: 341)
utslib.collection.history Closed (ID: 3)

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