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dc.contributor.authorHillhouse, Erin
dc.contributor.authorCollin, Roxanne
dc.contributor.authorChabot-Roy, Geneviève
dc.contributor.authorGuyon, Marie-Josée
dc.contributor.authorTessier, Nathalie
dc.contributor.authorBoulay, Maryse
dc.contributor.authorLiscourt, Patricia
dc.contributor.authorLesage, Sylvie
dc.date.accessioned2023-01-17T16:56:08Z
dc.date.availableNO_RESTRICTIONfr
dc.date.available2023-01-17T16:56:08Z
dc.date.issued2013
dc.identifier.urihttp://hdl.handle.net/1866/27327
dc.publisherHindawifr
dc.rightsAttribution 3.0 non transposé (CC BY 3.0)
dc.rights.urihttps://creativecommons.org/licenses/by/3.0/deed.fr
dc.titleNearby construction impedes the progression to overt autoimmune diabetes in NOD micefr
dc.typeArticlefr
dc.contributor.affiliationUniversité de Montréal. Faculté de médecine. Département de microbiologie, infectiologie et immunologiefr
dc.identifier.doi10.1155/2013/620313
dcterms.abstractConstruction nearby animal houses has sporadically been reported to affect various aspects of animal health. Most of the reports have focussed on the impact on stress hormone levels and the hypersensitivity of animals relative to humans. There has also been an anecdotal report on the impact of construction on autoimmune diabetes in NOD mice. Here, we describe that nearby construction significantly impedes the progression to overt diabetes in female NOD mice offspring. We demonstrate that this was not due to a genetic drift or to particularities associated with our specific mouse colony. Interestingly, although the glycemia levels remained low in mice born from mothers subject to construction stress during gestation, we detected an active autoimmune reaction towards pancreatic islet cells, as measured by both the degree of insulitis and the presence of insulin autoantibody levels in the serum. These results suggest that the external stress imposed during embryonic development does not prevent but significantly delays the autoimmune process. Together, our findings emphasize the impact of surrounding factors during in vivo studies and are in agreement with the hypothesis that both environmental and genetic cues contribute to autoimmune diabetes development.fr
dcterms.isPartOfurn:ISSN: 2314-6745fr
dcterms.isPartOfurn:ISSN:2314-6753fr
dcterms.languageengfr
UdeM.ReferenceFournieParDeposanthttps://doi.org/10.1155/2013/620313fr
UdeM.VersionRioxxVersion publiée / Version of Recordfr
oaire.citationTitleJournal of diabetes researchfr


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