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膳食磷、钙代谢与骨骼。

Dietary phosphorus, calcium metabolism and bone.

作者信息

Calvo M S

机构信息

Center for Food Safety and Applied Nutrition, Food and Drug Administration, Washington, DC 20204.

出版信息

J Nutr. 1993 Sep;123(9):1627-33. doi: 10.1093/jn/123.9.1627.

DOI:10.1093/jn/123.9.1627
PMID:8360792
Abstract

Many American women consume diets high in phosphorus and low in calcium. Concern about this dietary pattern stems from studies that show high phosphorus, low calcium intake causes secondary hyperparathyroidism and bone loss in several animal models. Recent studies in young adults have shown that a high phosphorus, moderately low calcium intake results in mild secondary hyperparathyroidism that persisted over 4 wk. However, plasma concentrations of the active form of vitamin D did not change in these subjects, despite stimulatory changes in parathyroid hormone and serum ionized calcium. Studies in normal adult men have shown that dietary phosphorus at levels within the observed normal range of intake can finely regulate the renal production and serum concentration of 1,25-dihydroxycholecalciferol. Thus, prolonged high phosphorus intake may impair the usual homeostatic mechanisms that are evoked when dietary calcium is limited. The current dietary patterns of high phosphorus, low calcium consumption result in persistent changes in the calcium regulating hormones that are not conductive to optimizing peak bone mass or slowing the rate of bone loss.

摘要

许多美国女性的饮食中磷含量高而钙含量低。对这种饮食模式的担忧源于多项研究,这些研究表明,在几种动物模型中,高磷、低钙摄入会导致继发性甲状旁腺功能亢进和骨质流失。最近针对年轻人的研究表明,高磷、适度低钙摄入会导致轻度继发性甲状旁腺功能亢进,并持续4周以上。然而,尽管甲状旁腺激素和血清离子钙有刺激性变化,但这些受试者体内活性维生素D的血浆浓度并未改变。对正常成年男性的研究表明,在观察到的正常摄入范围内的膳食磷水平可以精细调节肾脏生成和血清中1,25-二羟胆钙化醇的浓度。因此,长期高磷摄入可能会损害在膳食钙受限时常被激活的正常稳态机制。当前高磷、低钙的饮食模式导致钙调节激素持续变化,这不利于优化峰值骨量或减缓骨质流失速度。

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