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• W2022115389 abstract "We hypothesise that the risk of placental dysfunction/insufficiency rises cumulatively in response to several interdependent risk factors that convergently regulate 1,25-dihydroxyvitamin D (the biologically active form of vitamin D, [1,25-(OH)2D]) levels at the feto-maternal interface. These factors include; (i) disturbances in genetic or epigenetic regulation of one-carbon metabolism and/or vitamin D metabolism and (ii) insufficiency in maternal vitamin D or in dietary intake of micronutrients that are involved in one-carbon donation. We predict that the sub-optimal functioning of folate and vitamin D metabolic pathways, in concert, represents a potential novel risk pathway for adverse pregnancy outcomes. We base this prediction on five observations: evidence linking polymorphisms in genes regulating one-carbon donor production and vitamin D metabolism with adverse pregnancy outcomes involving placental dysfunction; evidence linking sub-optimal maternal levels of both one-carbon donor and 1,25-(OH)2D precursors to adverse pregnancy outcomes involving placental dysfunction; the requirement for adequate one-carbon donor molecules (produced solely from dietary sources) to establish epigenetic markings involving DNA methylation, in the developing placenta and fetus; the demonstrated modulation of vitamin D pathway regulatory genes by DNA methylation; and data demonstrating specific DNA methylation-induced epigenetic silencing of the 24-hydroxylase gene (CYP24A1), encoding the major catabolic enzyme of 1,25-(OH)2D, and 25-hydroxyvitamin D (25-(OH)2D) in the placenta. It is anticipated that this ‘uncouples’ vitamin D homeostasis at the feto-maternal interface, allowing accumulation of the higher levels of 1,25-(OH)2D seen in pregnancy. In order to test this model, future epidemiological studies aimed at identifying risk factors for disorders linked to sub-optimal placental development and functioning, should: (a) measure circulating precursor molecules (including folate, vitamin B12, homocysteine, and vitamin D) in maternal and cord blood; (b) collect samples for examination of genotypic variation in both one-carbon and vitamin D regulatory genes and, (c) collect samples for examination of epigenetic status of genes regulating vitamin D homeostasis and action in the placenta." @default.
• W2022115389 created "2016-06-24" @default.
• W2022115389 creator A5011738671 @default.
• W2022115389 creator A5026404275 @default.
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• W2022115389 date "2009-12-01" @default.
• W2022115389 modified "2023-09-23" @default.
• W2022115389 title "A convergent model for placental dysfunction encompassing combined sub-optimal one-carbon donor and vitamin D bioavailability" @default.
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• W2022115389 doi "https://doi.org/10.1016/j.mehy.2009.03.057" @default.
• W2022115389 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19819084" @default.
• W2022115389 hasPublicationYear "2009" @default.
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