Department of Human Nutrition, Faculty of Life Sciences, University of Copenhagen, Rolighedsvej 30 DK-1958 Frederiksberg C, Denmark.
Bone. 2010 Feb;46(2):432-9. doi: 10.1016/j.bone.2009.08.056. Epub 2009 Sep 6.
A high peak bone mass may be essential for reducing the risk of osteoporosis later in life and a sufficient vitamin D level during puberty may be necessary for optimal bone accretion and obtaining a high peak bone mass. Dietary intake and synthesis during winter of vitamin D might be limited but the effect of vitamin D supplementation in adolescence on bone mass is not well established.
To investigate the effect of supplementation with 5 and 10 microg/day vitamin D(3) for 12 months in 11- to 12-year-old girls on bone mass and bone turnover as well as the possible influence of VDR and ER genotype on the effect of the supplementation.
The girls (n=221) were randomized to receive either 5 microg or 10 microg vitamin D(3) supplementation per day or placebo for 12 months. Whole body and lumbar spine bone mass measured by DXA and pubertal status were determined at baseline and after 12 months whereas physical activity and dietary intake of calcium and vitamin D were assessed at baseline. Serum (S) 25-hydroxyvitamin D (25OHD), S-osteocalcin, S-parathyroid hormone, S-calcium, S-inorganic phosphate, urinary (U) pyridinoline (Pyr) and deoxpyridinoline (Dpyr) were measured at baseline and after 6 and 12 months.
The S-25OHD concentration increased (p<0.001) relative to the baseline values in the groups receiving either 5 microg/day (mean+/-SD; 11.0+/-10.3 nmol/l, baseline 41.9+/-17.6 nmol/l) or 10 microg/day (13.3+/-11.8 nmol/l, baseline 44.4+/-16.6 nmol/l) vitamin D(3) for 12 months compared to placebo (-3.1+/-9.8 nmol/l, baseline 43.4+/-17.1 nmol/l). There was no effect of vitamin D-supplementation on biomarkers for bone turnover or on whole body or spine bone mineral augmentation. However, vitamin D supplementation increased whole body bone mineral density (BMD) (p=0.007) and bone mineral content (BMC) (p=0.048) in the FF VDR genotype but not in the Ff or ff VDR genotypes.
Supplementation with vitamin D (5 or 10 microg/day) over 12 months increased the S-25OHD concentration but there was no effect on indices of bone health in the entire group of girls. However, there was an effect on BMD for a subgroup with the FF VDR genotype indicating an influence of genotype.
高峰值骨量可能对降低日后骨质疏松症的风险至关重要,青春期维生素 D 水平充足可能对最佳骨量积累和获得高峰值骨量至关重要。冬季维生素 D 的饮食摄入和合成可能会受到限制,但青春期补充维生素 D 对骨量的影响尚未得到充分证实。
研究 11-12 岁女孩每天补充 5 和 10 微克维生素 D(3)12 个月对骨量和骨转换的影响,以及 VDR 和 ER 基因型对补充效果的可能影响。
将 221 名女孩随机分为每天接受 5 微克或 10 微克维生素 D(3)补充或安慰剂治疗 12 个月。在基线和 12 个月时通过 DXA 测量全身和腰椎骨量,并确定青春期状态,同时在基线时评估钙和维生素 D 的饮食摄入和体力活动。在基线、6 个月和 12 个月时测量血清(S)25-羟维生素 D(25OHD)、S-骨钙素、S-甲状旁腺激素、S-钙、S-无机磷、尿(U)吡啶啉(Pyr)和脱氧吡啶啉(Dpyr)。
与安慰剂组(基线 43.4+/-17.1 nmol/l,-3.1+/-9.8 nmol/l)相比,每天接受 5 微克(平均+/-SD;11.0+/-10.3 nmol/l,基线 41.9+/-17.6 nmol/l)或 10 微克(13.3+/-11.8 nmol/l,基线 44.4+/-16.6 nmol/l)维生素 D(3)治疗 12 个月后,S-25OHD 浓度增加(p<0.001)。维生素 D 补充对骨转换的生物标志物或全身或脊柱骨矿物质增加均无影响。然而,维生素 D 补充增加了 FF VDR 基因型的全身骨密度(BMD)(p=0.007)和骨矿物质含量(BMC)(p=0.048),但在 Ff 或 ff VDR 基因型中则没有。
补充维生素 D(5 或 10 微克/天)12 个月可增加 S-25OHD 浓度,但对整个女孩组的骨健康指标没有影响。然而,对于具有 FF VDR 基因型的亚组,BMD 有影响,表明基因型有影响。