Interrelationship among vitamin D metabolism, true calcium absorption, parathyroid function, and age in women: Evidence of an age‐related intestinal resistance to 1,25‐dihydroxyvitamin D action
Interrelationship among vitamin D metabolism, true calcium absorption, parathyroid function, and age in women: Evidence of an age‐related intestinal resistance to 1,25‐dihydroxyvitamin D action
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DOI：
10.1002/jbmr.5650060205
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发表时间：
1991-02
影响因子：
6.2
通讯作者：
R. Eastell;A. Yergey;N. Vieira;S. L. Cedel;Rajiv Kumar-;B. Riggs
中科院分区：
文献类型：
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作者：
R. Eastell;A. Yergey;N. Vieira;S. L. Cedel;Rajiv Kumar-;B. Riggs
我们研究了51名年龄在26 ~ 88岁之间的健康女性随年龄增长而钙吸收受损的机制。血清中1，25-二羟维生素D [1，25-（OH）2D，每名受试者四次测量的平均值]浓度随年龄增加22%（P < 0.05），但通过分裂点分析，在65岁后达到稳定或略有下降。在一个由20名受试者组成的亚组中，[3 H] 1，25-（OH）2D 3动力学分析表明，这种随年龄增长的增加是由于1，25-（OH）2D的产生增加和代谢清除率降低所致。尽管血清1，25-（OH）2D浓度增加，但真正的钙吸收并不随年龄而变化。然而，预期的钙吸收率与膳食钙摄入量之间的负相关性很容易得到证实（r = 0.66，P < 0.001）。血清全段甲状旁腺激素（PTH）随增龄增加35%（P < 0.02），血清骨钙素（BGP）随增龄增加47%（P < 0.001），PTH与BGP呈正相关（r = 0.32，P < 0.05）。数据与以下假设模型一致：（1）肠道对1，25-（OH）2D作用的抵抗导致血清1，25-（OH）2D浓度随年龄增长而增加，而真正的钙吸收没有变化;（2）这导致PTH分泌和1，25-（OH）2D产生的代偿性增加，防止真正的钙吸收减少;（3）先前描述的老龄动物和人类25-羟基维生素D（25-OHD）1α-羟化酶活性缺陷导致65岁后血清1，25-（OH）2D浓度趋于平稳;（4）继发性甲状旁腺功能亢进导致骨转换增加，从而导致年龄相关性骨丢失。
We studied the mechanism of impaired calcium absorption with aging in 51 healthy women whose ages ranged from 26 to 88 years. Serum concentrations of 1,25‐dihydroxyvitamin D [1,25‐(OH)2D, mean of four measurements per subject] increased with age by 22% (P < 0.05) but, by split‐point analysis, plateaued or decreased slightly after age 65. In a subset of 20 subjects, [3H]1,25‐(OH)2D3 kinetic analysis showed that this increase with age resulted from both increased production and decreased metabolic clearance of 1,25‐(OH)2D. Despite the increase in serum 1,25‐(OH)2D concentration, true calcium absorption did not change with age. The expected inverse correlation between true fractional calcium absorption and dietary calcium intake, however, was easily demonstrated (r = 0.66, P < 0.001). Serum intact parathyroid hormone (PTH) increased with age by 35% (P < 0.02) and serum bone gla protein (BGP, osteocalcin) increased by 47% (P < 0.001); the increases in serum PTH and serum BGP were directly correlated (r = 0.32, P < 0.05). The data are consistent with the following hypothetical model: (1) intestinal resistance to 1,25‐(OH)2D action accounts for the increase in serum 1,25‐(OH)2D concentrations with aging with no change in true calcium absorption; (2) this results in a compensatory increase in PTH secretion and in 1,25‐(OH)2D production that prevents true calcium absorption from decreasing; (3) the previously described defect in 25‐hydroxyvitamin D (25‐OHD) 1α‐hydroxylase activity in aging animals and humans acccounts for the leveling off in serum 1,25‐(OH)2D concentration after age 65 years; and (4) the secondary hyperparathyroidism leads to increased bone turnover and thus contributes to age‐related bone loss.