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

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dc.contributor.author O'Brien, Bronwyn en_US
dc.contributor.author Harmon, Brian en_US
dc.contributor.author Cameron, Donald en_US
dc.contributor.author Allan, David en_US
dc.contributor.editor en_US
dc.date.accessioned 2012-02-10T06:09:18Z
dc.date.available 2012-02-10T06:09:18Z
dc.date.issued 1996 en_US
dc.identifier 2010003377 en_US
dc.identifier.citation O'Brien Bronwyn et al. 1996, 'Beta cell apoptosis is responsible for the development of IDDM in the multiple low-dose streptozotocin model', Wiley, vol. 178, pp. 176-181. en_US
dc.identifier.issn 0022-3417 en_US
dc.identifier.other C1UNSUBMIT en_US
dc.identifier.uri http://hdl.handle.net/10453/16981
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. en_US
dc.language en_US
dc.publisher Wiley en_US
dc.title Beta cell apoptosis is responsible for the development of IDDM in the multiple low-dose streptozotocin model en_US
dc.parent Journal Of Pathology en_US
dc.journal.volume 178 en_US
dc.journal.number en_US
dc.publocation UK en_US
dc.identifier.startpage 176 en_US
dc.identifier.endpage 181 en_US
dc.cauo.name SCI.Medical and Molecular Biosciences en_US
dc.conference Verified OK en_US
dc.for 110300 en_US
dc.personcode 030027 en_US
dc.personcode 0000069664 en_US
dc.personcode 0000069665 en_US
dc.personcode 0000069666 en_US
dc.percentage 100 en_US
dc.classification.name Clinical Sciences en_US
dc.classification.type FOR-08 en_US
dc.edition en_US
dc.custom en_US
dc.date.activity en_US
dc.location.activity en_US
dc.description.keywords apoptosis; streptozotocin; IDDM; mouse en_US
dc.staffid en_US


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