Maternal 25-hydroxyvitamin D is inversely correlated with foetal serotonin
Murthi P, Davies-Tuck M, Lappas M, Singh H, Mockler J, Rahman R, Lim R, Leaw B, Doery J, Wallace EM, Ebeling PR
Clinical endocrinology · 19 citas
Cómo se estudió
- Diseño
- Estudio transversal (clasificado por nuestro filtro de IA)
- Estudiado en
- Personas, más trabajo en animales o laboratorio
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- State Government of Victoria
- Gobierno
- Medical Research Council
- Gobierno
- National Health and Medical Research Council
- Universidad u hospital
- Australian Institute of Musculoskeletal Science
- Subvenciones
- National Health and Medical Research Council (1047025)
Según 4 financiadores declarados.
Publicación
- Publicado
- 2016-11-15 · Clin Endocrinol (Oxf) · vol. 86 · número 3 · págs. 401–409
- Editorial
- Wiley
- Citado
- 26 citas · más que el 88% de estudios similares · 2.3× el promedio de su campo
- Referencias
- 52 trabajos
- Acceso
- Lectura gratuita
- Áreas de investigación
- Vitamin D Research Studies · Maternal Mental Health During Pregnancy and Postpartum · Birth, Development, and Health
- Palabras clave
- Endocrinology, Serotonin, Internal medicine, Serotonergic, Vitamin D and neurology, Umbilical cord, Fetus, Calcitriol receptor, Medicine, Chemistry, Biology, Pregnancy, Receptor, Immunology
- MeSH
- cell line, fetal blood, humans, pregnancy complications, vitamin d deficiency, serotonin, vitamin d, mothers, pregnancy, maternal-fetal exchange, adult, infant, newborn, female, young adult, human umbilical vein endothelial cells
11 autores
- Padma Murthi🇦🇺Hudson Institute of Medical Research; Monash University
- Miranda L. Davies-Tuck🇦🇺Hudson Institute of Medical Research; Monash University
- Martha Lappas🇦🇺The University of Melbourne; Mercy Hospital for Women; Austin Health
- Harmeet Singh🇦🇺Hudson Institute of Medical Research
- Joanne C. Mockler🇦🇺Hudson Institute of Medical Research; Monash University
- Rahana Abd Rahman🇦🇺Hudson Institute of Medical Research; Monash University
- Rebecca Lim🇦🇺Hudson Institute of Medical Research
- Bryan Leaw🇦🇺Hudson Institute of Medical Research
- James C.G. Doery🇦🇺Monash Health
- Euan Morrison Wallace🇦🇺Hudson Institute of Medical Research; Monash University
- Peter Robert Ebeling🇦🇺 · autor de correspondenciaMonash University
Resumen
El texto original del estudio, en el idioma en que se publicó.
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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