School of Stomatology, Wuhan University, Hubei, China.
PLoS One. 2012;7(10):e47058. doi: 10.1371/journal.pone.0047058. Epub 2012 Oct 8.
Epidemiologic studies correlate low vitamin C intake with bone loss. The genetic deletion of enzymes involved in de novo vitamin C synthesis in mice, likewise, causes severe osteoporosis. However, very few studies have evaluated a protective role of this dietary supplement on the skeleton. Here, we show that the ingestion of vitamin C prevents the low-turnover bone loss following ovariectomy in mice. We show that this prevention in areal bone mineral density and micro-CT parameters results from the stimulation of bone formation, demonstrable in vivo by histomorphometry, bone marker measurements, and quantitative PCR. Notably, the reductions in the bone formation rate, plasma osteocalcin levels, and ex vivo osteoblast gene expression 8 weeks post-ovariectomy are all returned to levels of sham-operated controls. The study establishes vitamin C as a skeletal anabolic agent.
流行病学研究表明，维生素 C 摄入不足与骨量流失有关。同样，在小鼠中，参与从头合成维生素 C 的酶的基因缺失也会导致严重的骨质疏松症。然而，很少有研究评估这种膳食补充剂对骨骼的保护作用。在这里，我们表明，维生素 C 的摄入可预防去卵巢小鼠的低转换骨丢失。我们表明，这种对面积骨密度和 micro-CT 参数的预防作用源自骨形成的刺激，通过组织形态计量学、骨标志物测量和定量 PCR 在体内得到证明。值得注意的是，去卵巢 8 周后骨形成率、血浆骨钙素水平和体外成骨细胞基因表达的降低均恢复到假手术对照组的水平。该研究确立了维生素 C 作为一种骨骼合成代谢剂。
