Maternal 25-hydroxyvitamin D is inversely correlated with foetal serotonin

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

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

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 siRNA knockdown of the vitamin D receptor (VDR) and administration of 10 nm 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 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.

Original languageEnglish
JournalClinical Endocrinology
DOIs
Publication statusAccepted/In press - 2016
Externally publishedYes

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Serotonin
Mothers
Human Umbilical Vein Endothelial Cells
Calcitriol Receptors
Vitamin D Deficiency
Calcitriol
Vitamin D
25-hydroxyvitamin D
Fetal Development
Fetal Blood
Small Interfering RNA
Neurotransmitter Agents
Linear Models
Pregnancy
Brain

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism

Cite this

Murthi, P., Davies-Tuck, M., Lappas, M., Singh, H., Mockler, J., Abd Rahman, R., ... Ebeling, P. R. (Accepted/In press). Maternal 25-hydroxyvitamin D is inversely correlated with foetal serotonin. Clinical Endocrinology. https://doi.org/10.1111/cen.13281

Maternal 25-hydroxyvitamin D is inversely correlated with foetal serotonin. / Murthi, Padma; Davies-Tuck, Miranda; Lappas, Martha; Singh, Harmeet; Mockler, Joanne; Abd Rahman, Rahana; Lim, Rebecca; Leaw, Bryan; Doery, James; Wallace, Euan M.; Ebeling, Peter R.

In: Clinical Endocrinology, 2016.

Research output: Contribution to journalArticle

Murthi, P, Davies-Tuck, M, Lappas, M, Singh, H, Mockler, J, Abd Rahman, R, Lim, R, Leaw, B, Doery, J, Wallace, EM & Ebeling, PR 2016, 'Maternal 25-hydroxyvitamin D is inversely correlated with foetal serotonin', Clinical Endocrinology. https://doi.org/10.1111/cen.13281
Murthi, Padma ; Davies-Tuck, Miranda ; Lappas, Martha ; Singh, Harmeet ; Mockler, Joanne ; Abd Rahman, Rahana ; Lim, Rebecca ; Leaw, Bryan ; Doery, James ; Wallace, Euan M. ; Ebeling, Peter R. / Maternal 25-hydroxyvitamin D is inversely correlated with foetal serotonin. In: Clinical Endocrinology. 2016.
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AU - Murthi, Padma

AU - Davies-Tuck, Miranda

AU - Lappas, Martha

AU - Singh, Harmeet

AU - Mockler, Joanne

AU - Abd Rahman, Rahana

AU - Lim, Rebecca

AU - Leaw, Bryan

AU - Doery, James

AU - Wallace, Euan M.

AU - Ebeling, Peter R.

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N2 - 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 siRNA knockdown of the vitamin D receptor (VDR) and administration of 10 nm 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 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.

AB - 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 siRNA knockdown of the vitamin D receptor (VDR) and administration of 10 nm 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 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.

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