Maternal vitamin D deficiency during rat gestation elicits a milder phenotype compared to the mouse model: Implications for the placental glucocorticoid barrier

Research output: Contribution to journalArticle

Abstract

Maternal vitamin D deficiency disturbs fetal development and programmes neurodevelopmental complications in offspring, possibly through increased fetal glucocorticoid exposure. We aimed to determine whether prenatal exposure to excess glucocorticoids underlies our rat model of early-life vitamin D deficiency, leading to altered adult behaviours. Vitamin D deficiency reduced the expression of the glucocorticoid-inactivating enzyme Hsd11b2 in the female placenta, but did not alter maternal glucocorticoid levels, feto-placental weights, or placental expression of other glucocorticoid-related genes at mid-gestation. This differs to the phenotype previously observed in vitamin D deficient mice, and highlights important modelling considerations.

Original languageEnglish
Pages (from-to)5-7
Number of pages3
JournalPlacenta
Volume83
DOIs
Publication statusPublished - Aug 2019

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Vitamin D Deficiency
Glucocorticoids
Mothers
Phenotype
Pregnancy
Fetal Development
Vitamin D
Placenta
Weights and Measures
Enzymes
Genes

Cite this

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title = "Maternal vitamin D deficiency during rat gestation elicits a milder phenotype compared to the mouse model: Implications for the placental glucocorticoid barrier",
abstract = "Maternal vitamin D deficiency disturbs fetal development and programmes neurodevelopmental complications in offspring, possibly through increased fetal glucocorticoid exposure. We aimed to determine whether prenatal exposure to excess glucocorticoids underlies our rat model of early-life vitamin D deficiency, leading to altered adult behaviours. Vitamin D deficiency reduced the expression of the glucocorticoid-inactivating enzyme Hsd11b2 in the female placenta, but did not alter maternal glucocorticoid levels, feto-placental weights, or placental expression of other glucocorticoid-related genes at mid-gestation. This differs to the phenotype previously observed in vitamin D deficient mice, and highlights important modelling considerations.",
keywords = "Glucocorticoids, Placenta, Vitamin D",
author = "Crew, {Rachael C.} and Ana Rakonjac and Dijana Tesic and Clarke, {Michael W.} and Yates, {Nathanael J.} and Wyrwoll, {Caitlin S.}",
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AU - Crew, Rachael C.

AU - Rakonjac, Ana

AU - Tesic, Dijana

AU - Clarke, Michael W.

AU - Yates, Nathanael J.

AU - Wyrwoll, Caitlin S.

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AB - Maternal vitamin D deficiency disturbs fetal development and programmes neurodevelopmental complications in offspring, possibly through increased fetal glucocorticoid exposure. We aimed to determine whether prenatal exposure to excess glucocorticoids underlies our rat model of early-life vitamin D deficiency, leading to altered adult behaviours. Vitamin D deficiency reduced the expression of the glucocorticoid-inactivating enzyme Hsd11b2 in the female placenta, but did not alter maternal glucocorticoid levels, feto-placental weights, or placental expression of other glucocorticoid-related genes at mid-gestation. This differs to the phenotype previously observed in vitamin D deficient mice, and highlights important modelling considerations.

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