Vitamin D deficiency and impaired placental function: Potential regulation by glucocorticoids?

Research output: Contribution to journalReview article

13 Citations (Scopus)

Abstract

Maternal vitamin D deficiency has been implicated in a range of pregnancy complications including preeclampsia, preterm birth and intrauterine growth restriction. Some of these adverse outcomes arise from alterations in placental function. Indeed, vitamin D appears critical for implantation, inflammation, immune function and angiogenesis in the placenta. Despite these associations, absence of the placental vitamin D receptor in mice provokes little effect. Thus, interactions between maternal and fetal compartments are likely crucial for instigating adverse placental changes. Indeed, maternal vitamin D deficiency elicits changes in glucocorticoid-related parameters in pregnancy, which increase placental and fetal glucocorticoid exposure. As in utero glucocorticoid excess has a well-established role in eliciting placental dysfunction and fetal growth restriction, this review proposes that glucocorticoids are an important consideration when understanding the impact of vitamin D deficiency on placental function and fetal development.

Original languageEnglish
Pages (from-to)R163-R171
JournalReproduction
Volume153
Issue number5
DOIs
Publication statusPublished - 2017

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Vitamin D Deficiency
Glucocorticoids
Mothers
Fetal Development
Placentation
Calcitriol Receptors
Pregnancy Complications
Premature Birth
Pre-Eclampsia
Vitamin D
Placenta
Inflammation
Pregnancy
Growth

Cite this

@article{2d1d0879b87f494abc640b8fac597a6c,
title = "Vitamin D deficiency and impaired placental function: Potential regulation by glucocorticoids?",
abstract = "Maternal vitamin D deficiency has been implicated in a range of pregnancy complications including preeclampsia, preterm birth and intrauterine growth restriction. Some of these adverse outcomes arise from alterations in placental function. Indeed, vitamin D appears critical for implantation, inflammation, immune function and angiogenesis in the placenta. Despite these associations, absence of the placental vitamin D receptor in mice provokes little effect. Thus, interactions between maternal and fetal compartments are likely crucial for instigating adverse placental changes. Indeed, maternal vitamin D deficiency elicits changes in glucocorticoid-related parameters in pregnancy, which increase placental and fetal glucocorticoid exposure. As in utero glucocorticoid excess has a well-established role in eliciting placental dysfunction and fetal growth restriction, this review proposes that glucocorticoids are an important consideration when understanding the impact of vitamin D deficiency on placental function and fetal development.",
author = "Nathanael Yates and Crew, {Rachael C.} and Wyrwoll, {Caitlin S.}",
year = "2017",
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volume = "153",
pages = "R163--R171",
journal = "Journal of Reproduction and Fertility",
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TY - JOUR

T1 - Vitamin D deficiency and impaired placental function

T2 - Potential regulation by glucocorticoids?

AU - Yates, Nathanael

AU - Crew, Rachael C.

AU - Wyrwoll, Caitlin S.

PY - 2017

Y1 - 2017

N2 - Maternal vitamin D deficiency has been implicated in a range of pregnancy complications including preeclampsia, preterm birth and intrauterine growth restriction. Some of these adverse outcomes arise from alterations in placental function. Indeed, vitamin D appears critical for implantation, inflammation, immune function and angiogenesis in the placenta. Despite these associations, absence of the placental vitamin D receptor in mice provokes little effect. Thus, interactions between maternal and fetal compartments are likely crucial for instigating adverse placental changes. Indeed, maternal vitamin D deficiency elicits changes in glucocorticoid-related parameters in pregnancy, which increase placental and fetal glucocorticoid exposure. As in utero glucocorticoid excess has a well-established role in eliciting placental dysfunction and fetal growth restriction, this review proposes that glucocorticoids are an important consideration when understanding the impact of vitamin D deficiency on placental function and fetal development.

AB - Maternal vitamin D deficiency has been implicated in a range of pregnancy complications including preeclampsia, preterm birth and intrauterine growth restriction. Some of these adverse outcomes arise from alterations in placental function. Indeed, vitamin D appears critical for implantation, inflammation, immune function and angiogenesis in the placenta. Despite these associations, absence of the placental vitamin D receptor in mice provokes little effect. Thus, interactions between maternal and fetal compartments are likely crucial for instigating adverse placental changes. Indeed, maternal vitamin D deficiency elicits changes in glucocorticoid-related parameters in pregnancy, which increase placental and fetal glucocorticoid exposure. As in utero glucocorticoid excess has a well-established role in eliciting placental dysfunction and fetal growth restriction, this review proposes that glucocorticoids are an important consideration when understanding the impact of vitamin D deficiency on placental function and fetal development.

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U2 - 10.1530/REP-16-0647

DO - 10.1530/REP-16-0647

M3 - Review article

VL - 153

SP - R163-R171

JO - Journal of Reproduction and Fertility

JF - Journal of Reproduction and Fertility

SN - 0022-4251

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ER -