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Maternal 25‐hydroxyvitamin D is inversely correlated with foetal serotonin
Author(s) -
Murthi Padma,
DaviesTuck Miranda,
Lappas Martha,
Singh Harmeet,
Mockler Joanne,
Rahman Rahana,
Lim Rebecca,
Leaw Bryan,
Doery James,
Wallace Euan M.,
Ebeling Peter R.
Publication year - 2017
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/cen.13281
Subject(s) - endocrinology , serotonin , medicine , serotonergic , vitamin d and neurology , umbilical cord , fetus , calcitriol receptor , chemistry , biology , pregnancy , receptor , immunology , genetics
Summary 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 foetal brain development. In this study, we aimed to explore associations between maternal and foetal vitamin D concentrations, and foetal serotonin concentrations at term. Study design and measurements Serum 25‐hydroxyvitamin 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 si RNA knockdown of the vitamin D receptor ( VDR ) and administration of 10 n m 1,25‐dihydroxyvitamin D 3 on serotonin secretion in human umbilical vein endothelial cells ( HUVEC s) in vitro . Results We observed an inverse relationship between both maternal and cord 25( OH )D concentrations with cord serotonin concentrations. The treatment of HUVEC s with 1,25‐dihydroxyvitamin D 3 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 HUVEC s. Conclusions These observations provide the first evidence of an inverse relationship between maternal 25( OH )D and foetal serotonin concentrations. We propose that maternal vitamin D deficiency increases foetal serotonin concentrations and thereby contributes to longer‐term neurocognitive impairment in infants and children.