Am J Clin Nutr 72:690–693PubMed 38. Tangpricha V, Koutkia P, Rieke SM, Chen TC, Perez AA, Holick MF (2003) Fortification of orange juice with vitamin D: a novel approach for enhancing vitamin D nutritional health. Am J Clin Nutr 77:1478–1483PubMed
39. Natri AM, Salo P, Vikstedt T, Palssa A, Huttunen M, Karkkainen MU, Salovaara H, Piironen V, Jakobsen J, Lamberg-Allardt CJ (2006) Bread fortified with cholecalciferol increases the serum 25-hydroxyvitamin D concentration in women as effectively as a cholecalciferol supplement. J Nutr 136:123–127PubMed”
“Introduction Poor growth during the fetal period, infancy and early childhood is associated with lower adult INK 128 manufacturer bone mass and increased fracture risk later in life [1–3]. During the fetal period, it is likely that metabolic and endocrine systems are programmed to allow the fetus to adapt to the in utero environment [4]. Vitamin D is a seco sterol that modifies various biological functions in the body [5], and researchers have identified 37 target organs for vitamin D [5]. Low maternal vitamin D status
or inadequate dietary vitamin D intake during pregnancy predisposes children to asthma and allergic rhinitis [6], diabetes [7], acute lower respiratory infection [8], and impaired bone mass accrual. This is evidenced by smaller bone cross-sectional area (CSA) and bone mineral content (BMC) at birth [9, 10] and at 9 years of age [11]. Programming of skeletal growth may occur through growth hormone—IGF-I axis [4, 12], whereas bone quality may be determined by factors related to differentiation of mesenchymal stem cells [13, 14]. The intrauterine environment strongly affects growth Copanlisib cost rate in infancy, but may also influence growth in puberty [15]. The extent to which changes in nutrient supply 4��8C between intrauterine and postnatal periods affect growth and development, per se, has not been well established [4]. The most critical views
predict that intrauterine nutritional deficits have permanent consequences and that a newborn’s metabolism may not adapt to improved nutritional status; the nutrients may not be utilized efficiently and the risk for disease may be maintained despite improved nutritional status [16]. However, postnatal catch-up occurs in linear growth if the fetal deprivation and its timing and magnitude have not been too critical [17]. Previously the authors of the current study have reported that during the pregnancy, 69% of the women and 37% of the newborns at birth were vitamin D deficient (defined in women as S-25-OHD <50 nmol/l [18, 19] and in the newborn as <37.5 nmol/l [20]). The newborn bone variables were measured with peripheral quantitative computed tomography (pQCT) during the hospital stay. Based on these results, it was concluded that maternal vitamin D status affects bone mineral accrual and influences bone size during the intrauterine period [10]. The present prospective study had two objectives.