Abstract Title:

Maternal 25-hydroxyvitamin D is inversely correlated with fetal serotonin.

Abstract Source:

Clin Endocrinol (Oxf). 2016 Nov 12. Epub 2016 Aug 12. PMID: 27862146

Abstract Author(s):

Padma Murthi, Miranda Davies-Tuck, Martha Lappas, Harmeet Singh, Joanne Mockler, Rahana Rahman, Rebecca Lim, Bryan Leaw, James Doery, Euan M Wallace, Peter R Ebeling

Article Affiliation:

Padma Murthi


OBJECTIVE: Maternal vitamin D deficiency during pregnancy has been linked to impaired neurocognitive development in childhood. The mechanism by which vitamin D affects childhood neurocognition is unclear but may be via interactions with serotonin, a neurotransmitter involved in fetal brain development. In this study we aimed to explore associations between maternal and fetal vitamin D concentrations, and fetal serotonin concentrations at term.

STUDY DESIGN AND MEASUREMENTS: Serum 25-hydroxyitamin D (25(OH)D, nmol/L) and serotonin (5-HT, nmol/L) concentrations were measured in maternal and umbilical cord blood from mother-infant pairs (n=64). Association between maternal 25(OH)D, cord 25(OH)D and cord serotonin was explored using linear regression, before and after adjusting for maternal serotonin levels. We also assessed the effects of siRNA knockdown of the vitamin D receptor (VDR) and administration of 10nM 1,25-dihydroxyvitamin D3 on serotonin secretion in human umbilical vein endothelial cells (HUVECs) in vitro.

RESULTS: We observed an inverse relationship between both maternal and cord 25(OH)D concentrations with cord serotonin concentrations. The treatment of HUVECs with 1,25- dihydroxyvitamin D3 in vitro decreased the release of serotonin (193·9±14·8 nmol/L vs. 458·9±317·5 nmol/L, control, p<0·05). Conversely, inactivation of VDR increased serotonin release in cultured HUVECs.

CONCLUSIONS: These observations provide the first evidence of an inverse relationship between maternal 25(OH)D and fetal serotonin concentrations. We propose that maternal vitamin D deficiency increases fetal serotonin concentrations and thereby contributes to longer-term neurocognitive impairment in infants and children. This article is protected by copyright. All rights reserved.

Study Type : Human Study

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