VITAMIN K AND BONE TURNOVER IN POSTMENOPAUSAL WOMEN

越来越多的数据表明，维生素K (K)不足可能会导致骨质流失，从而导致骨质疏松症的发生。然而，目前可用的数据不允许得出关于K在骨代谢中的作用的明确结论。许多证据表明，钾与骨骼健康有关，利用血清羧化骨钙素（ucOC）的测量作为钾状态的敏感指标。当ucOC升高被用来定义钾不足时，不足是非常常见的。然而，这种“营养不足”是否与骨骼相关，或者ucOC浓度升高只是普遍营养不足的替代，目前尚不清楚。为了阐明钾素不足在骨骼健康中的作用，我们建议在226名绝经后妇女中进行一项为期14个月的前瞻性、随机、双盲、安慰剂对照试验。我们假设补充K1可以减少骨骼更新。为了验证这一假设，我们将使用能最大限度降低血清ucOC的K1剂量（1000微克/天）。我们的具体目标是通过测定血清骨钙素、骨特异性碱性磷酸酶、l型胶原的n -端肽以及尿吡啶啉和脱氧吡啶啉来评估骨骼更新。如果钾缺乏导致高骨转换（已知的低骨量和骨质疏松性骨折的危险因素），建议的钾摄入量应该增加，补充K1应成为标准预防医疗保健的一部分。

Accumulating data suggest that vitamin K (K) insufficiency may contribute to osteoporosis development by causing by causing increased bone turnover. However, currently available data do not permit definitive conclusions to be drawn regarding a role of K in bone metabolism. Much of the evidence implicating K in bone health utilizes measurement of serum undercarboxylated osteocalcin (ucOC) as a sensitive indicator of K status. When ucOC elevation is used to define K inadequacy, insufficiency is extremely common. However, whether this "insufficiency has skeletal relevance, or if elevated ucOC concentration is simply a surrogate for generalized inadequate nutrition, is unknown. To clarify the role of K insufficiency in skeletal health, we propose a 14 month, prospective, randomized, double-blind, placebo controlled trial of K1 supplementation in 226 postmenopausal women. We hypothesize that K1 supplementation reduces skeletal turnover. To test this hypothesis we will use a K1 dose (1000 mcg/day) that produces maximal reduction in serum ucOC. Our specific objective is to assess skeletal turnover by measuring serum osteocalcin, bone specific alkaline phosphatase, and N-telopeptides of type l collagen, as well as urinary pyridinoline and deoxypyridinoline. If K insufficiency causes high bone turnover, a known risk factor for low bone mass and osteoporotic fracture, the recommended K intake should be increased and K1 supplementation become part of standard preventative medical care.