dc.contributor.author | Størdal, Ketil | en_US |
dc.contributor.author | McArdle, Harry J. | en_US |
dc.contributor.author | Hayes, Helen | en_US |
dc.contributor.author | Tapia, German | en_US |
dc.contributor.author | Viken, Marte K | en_US |
dc.contributor.author | Lund-Blix, Nicolai Andre | en_US |
dc.contributor.author | Haugen, Margaretha | en_US |
dc.contributor.author | Joner, Geir | en_US |
dc.contributor.author | Skrivarhaug, Torild | en_US |
dc.contributor.author | Mårild, Karl Staffan | en_US |
dc.contributor.author | Njølstad, Pål Rasmus | en_US |
dc.contributor.author | Eggesbø, Merete Åse | en_US |
dc.contributor.author | Mandal, Siddhartha | en_US |
dc.contributor.author | Page, Christian | en_US |
dc.contributor.author | London, Stephanie J. | en_US |
dc.contributor.author | Lie, Benedicte Alexandra | en_US |
dc.contributor.author | Stene, Lars Christian Mørch | en_US |
dc.date.accessioned | 2019-06-07T11:33:23Z | |
dc.date.available | 2019-06-07T11:33:23Z | |
dc.date.issued | 2018-06-13 | |
dc.Published | Størdal K, McArdle, Hayes, Tapia G, Viken MK, Lund-Blix NA, Haugen M, Joner GJ, Skrivarhaug T, Mårild K, Njølstad PR, Eggesbø MÅ, Mandal S, Page C, London SJ, Lie BA, Stene LC. Prenatal iron exposure and childhood type 1 diabetes. Scientific Reports. 2018;8:9067 | eng |
dc.identifier.issn | 2045-2322 | |
dc.identifier.uri | https://hdl.handle.net/1956/19917 | |
dc.description.abstract | Iron overload due to environmental or genetic causes have been associated diabetes. We hypothesized that prenatal iron exposure is associated with higher risk of childhood type 1 diabetes. In the Norwegian Mother and Child cohort study (n = 94,209 pregnancies, n = 373 developed type 1 diabetes) the incidence of type 1 diabetes was higher in children exposed to maternal iron supplementation than unexposed (36.8/100,000/year compared to 28.6/100,000/year, adjusted hazard ratio 1.33, 95%CI: 1.06–1.67). Cord plasma biomarkers of high iron status were non-significantly associated with higher risk of type 1 diabetes (ferritin OR = 1.05 [95%CI: 0.99–1.13] per 50 mg/L increase; soluble transferrin receptor: OR = 0.91 [95%CI: 0.81–1.01] per 0.5 mg/L increase). Maternal but not fetal HFE genotypes causing high/intermediate iron stores were associated with offspring diabetes (odds ratio: 1.45, 95%CI: 1.04, 2.02). Maternal anaemia or non-iron dietary supplements did not significantly predict type 1 diabetes. Perinatal iron exposures were not associated with cord blood DNA genome-wide methylation, but fetal HFE genotype was associated with differential fetal methylation near HFE. Maternal cytokines in mid-pregnancy of the pro-inflammatory M1 pathway differed by maternal iron supplements and HFE genotype. Our results suggest that exposure to iron during pregnancy may be a risk factor for type 1 diabetes in the offspring. | en_US |
dc.language.iso | eng | eng |
dc.publisher | Springer Nature | eng |
dc.relation.uri | https://www.nature.com/articles/s41598-018-27391-4.pdf | |
dc.rights | Attribution CC BY | eng |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0 | eng |
dc.title | Prenatal iron exposure and childhood type 1 diabetes | en_US |
dc.type | Peer reviewed | |
dc.type | Journal article | |
dc.date.updated | 2019-02-07T13:45:19Z | |
dc.description.version | publishedVersion | en_US |
dc.rights.holder | Copyright 2018 The Author(s) | |
dc.identifier.doi | https://doi.org/10.1038/s41598-018-27391-4 | |
dc.identifier.cristin | 1597062 | |
dc.source.journal | Scientific Reports | |