Vitamin D deficiency and impaired placental function: potential regulation by glucocorticoids?. Issue 5 (May 2017)

• Record Type: Journal Article
• Authors: Yates, Nathanael; Crew, Rachael C; Wyrwoll, Caitlin S
• Is Part Of: Reproduction. Volume 153:Issue 5(2017)
• Page Start: R163
• Page End: R171
• Publication Date: 2017-05
• Subjects: Reproduction -- Periodicals; Reproduction -- Molecular aspects -- Periodicals; Reproduction -- Immunological aspects -- Periodicals; Reproduction -- Endocrine aspects -- Periodicals; Fertility -- Periodicals; Human reproduction -- Periodicals; 571.805
• DOI: 10.1530/REP-16-0647
• Languages: English
• ISSNs: 1470-1626

Abstract

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.