Harvey, N.C., Martin, R., Javaid, M.K, Swaminathan, R., Taylor, P., Poole, J.R., Arden, N.K, Dennison, E.M., Inskip, H.M., Godfrey, K., Lewis, R.M. and Cooper, C. (2006) Maternal 25(OH)-vitamin D status in late pregnancy and mRNA expression of placental calcium transporter predict intrauterine bone mineral accrual in the offspring. Osteoporosis International, 17 (Supplement 2), S9 (OC9). (doi:10.1007/s00198-006-0096-z).
Abstract
Aims: Evidence suggests that intrauterine bone mineral accrual predicts osteoporosis risk in later life, and that maternal 25(OH)-vitamin D status in pregnancy is a determinant of neonatal bone mass. We aimed to explore the relationship between intrauterine bone mineral accrual in the offspring, and 1) maternal 25(OH)-vitamin D status during late pregnancy, and 2) expression of
calcium transporters in the placenta.
Methods: Pregnancies were recruited from the Southampton Women’s Survey, a unique, ongoing, well established cohort of women, aged 20–34 years, assessed before and during pregnancy. Maternal 25(OH)-vitamin D status was measured by radioimmunoassay in late pregnancy (34 weeks); the healthy, term, neonates underwent whole body (WB) DXA within 20 days of birth, using a Lunar DPX instrument. Placental samples, snap frozen in liquid nitrogen within 30 minutes of birth, were available for 70 of the pregnancies. A quantitative real time polymerase chain reaction was used to measure the mRNA expression of PMCA isoforms 1, 3 and 4 in the placenta, using beta-actin as a control gene.
Results: 556 (286 males) neonates were studied. Offspring of mothers who were deficient (<33nmol/l) in 25(OH)-vitamin D in late pregnancy had lower bone mass than those of replete mothers. Thus the mean WB bone area (BA) of the female offspring of 25(OH)-vitamin D deficient mothers was 110cm2 vs 119cm2 in offspring of replete mothers (p=0.04). The mean WB bone mineral content (BMC) for offspring of deficient vs replete mothers was 58g vs 63g (p=0.04), respectively. The relationships in the boys did not reach statistical significance. There was no association with maternal alkaline phosphatase. After controlling for beta-actin expression, PMCA3 mRNA expression predicted neonatal WB BA (r=0.28,p=0.02), WB BMC (r=0.25,p=0.04), placental weight (r=0.26,p=0.03), and birth weight (r=0.33,p=0.006).
Conclusions: These data are consistent with previous findings that mothers deficient in 25(OH)-vitamin D in pregnancy have children with reduced bone mass. The mechanism underlying this process may be explained, in part, by the demonstrated association between expression of the placental calcium transporter PMCA3 and neonatal whole body bone mineral content. Further elucidation of this process may allow development of novel therapeutic strategies to optimise childhood bone mineral accrual and thus reduce osteoporotic fractures in future generations.
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