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dc.contributor.authorHjort, Rebecka
dc.contributor.authorAhlqvist, Emma
dc.contributor.authorCarlsson, Per-Ola
dc.contributor.authorGrill, Valdemar Erik Robert
dc.contributor.authorGroop, Leif
dc.contributor.authorMartinell, Mats
dc.contributor.authorRasouli, Bahareh
dc.contributor.authorRosengren, Anders
dc.contributor.authorTuomi, Tiinamaija
dc.contributor.authorÅsvold, Bjørn Olav
dc.contributor.authorCarlsson, Sofia
dc.date.accessioned2019-03-14T07:34:20Z
dc.date.available2019-03-14T07:34:20Z
dc.date.created2018-07-02T13:21:44Z
dc.date.issued2018
dc.identifier.citationDiabetologia. 2018, 61 (6), 1333-1343.nb_NO
dc.identifier.issn0012-186X
dc.identifier.urihttp://hdl.handle.net/11250/2589921
dc.description.abstractAims/hypothesis Excessive weight is a risk factor for type 2 diabetes, but its role in the promotion of autoimmune diabetes is not clear. We investigated the risk of latent autoimmune diabetes in adults (LADA) in relation to overweight/obesity in two large population-based studies. Methods Analyses were based on incident cases of LADA (n = 425) and type 2 diabetes (n = 1420), and 1704 randomly selected control participants from a Swedish case–control study and prospective data from the Norwegian HUNT Study including 147 people with LADA and 1,012,957 person-years of follow-up (1984–2008). We present adjusted ORs and HRs with 95% CI. Results In the Swedish data, obesity was associated with an increased risk of LADA (OR 2.93, 95% CI 2.17, 3.97), which was even stronger for type 2 diabetes (OR 18.88, 95% CI 14.29, 24.94). The association was stronger in LADA with low GAD antibody (GADA;nb_NO
dc.language.isoengnb_NO
dc.publisherSpringer Verlagnb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleOverweight, obesity and the risk of LADA: results from a Swedish case-control study and the Norwegian HUNT Studynb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.description.versionpublishedVersionnb_NO
dc.source.pagenumber1333-1343nb_NO
dc.source.volume61nb_NO
dc.source.journalDiabetologianb_NO
dc.source.issue6nb_NO
dc.identifier.doi10.1007/s00125-018-4596-0
dc.identifier.cristin1595190
dc.description.localcode© The Author(s) 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/),nb_NO
cristin.unitcode194,65,15,0
cristin.unitcode194,65,20,0
cristin.unitnameInstitutt for klinisk og molekylær medisin
cristin.unitnameInstitutt for samfunnsmedisin og sykepleie
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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