Portale A A, Halloran B P, Murphy M M, Morris R C
J Clin Invest. 1986 Jan;77(1):7-12. doi: 10.1172/JCI112304.
Changes in the oral intake of phosphorus could induce the reported changes in the serum concentration of 1,25-dihydroxyvitamin D (1,25-(OH)2D) by inducing changes in its production rate (PR) or metabolic clearance rate (MCR), or both. To investigate these possibilities, we employed the constant infusion equilibrium technique to measure the PR and MCR of 1,25-(OH)2D in six healthy men in whom the oral intake of phosphorus was initially maintained at 1,500 mg/70 kg body weight per d for 9 d, then restricted to 500 mg/d (coupled with oral administration of aluminum hydroxide) for 10 d, and then supplemented to 3,000 mg/d for 10 d. With phosphorus restriction, the serum concentration of 1,25-(OH)2D increased by 80% from a mean of 38 +/- 3 to 68 +/- 6 pg/ml, P less than 0.001; the PR increased from 1.8 +/- 0.2 to 3.8 +/- 0.6 micrograms/d, P less than 0.005; the MCR did not change significantly. The fasting serum concentration of phosphorus decreased from 3.5 +/- 0.2 to 2.6 +/- 0.2 mg/dl, P less than 0.01. With phosphorus supplementation, the serum concentration of 1,25-(OH)2D decreased abruptly, reaching a nadir within 2 to 4 d; after 10 d of supplementation, the mean concentration of 27 +/- 4 pg/ml was lower by 29%, P less than 0.01, than the value measured when phosphorus intake was normal. The PR decreased to 1.3 +/- 0.2 micrograms/d, P less than 0.05; the MCR did not change significantly. The fasting serum concentration of phosphorus increased significantly, but only initially. These data demonstrate that in healthy men, reductions and increases in the oral intake of phosphorus can induce rapidly occurring, large, inverse, and persisting changes in the serum concentration of 1,25-(OH)2D. Changes in the PR of 1,25-(OH)2D account entirely for the phosphorus-induced changes in serum concentration of this hormone.
磷摄入量的变化可能通过诱导1,25 - 二羟基维生素D（1,25-(OH)₂D）的生成率（PR）或代谢清除率（MCR）或两者的变化，来引发所报道的血清浓度变化。为了探究这些可能性，我们采用持续输注平衡技术来测量6名健康男性体内1,25-(OH)₂D的PR和MCR。这些男性最初磷的口服摄入量维持在1500毫克/70千克体重/天，持续9天，然后限制在500毫克/天（同时口服氢氧化铝），持续10天，随后补充至3000毫克/天，持续10天。随着磷摄入受限，1,25-(OH)₂D的血清浓度从平均38±3皮克/毫升增加了80%，达到68±6皮克/毫升，P<0.001；PR从1.8±0.2微克/天增加到3.8±0.6微克/天，P<0.005；MCR没有显著变化。空腹血清磷浓度从3.5±0.2毫克/分升降至2.6±0.2毫克/分升，P<0.01。随着磷补充，1,25-(OH)₂D的血清浓度迅速下降，在2至4天内降至最低点；补充10天后，平均浓度为27±4皮克/毫升，比磷摄入量正常时测得的值低29%，P<0.01。PR降至1.3±0.2微克/天，P<0.05；MCR没有显著变化。空腹血清磷浓度显著升高，但仅在最初阶段。这些数据表明，在健康男性中，磷摄入量的减少和增加可诱导1,25-(OH)₂D血清浓度迅速出现大幅反向且持续的变化。1,25-(OH)₂D的PR变化完全解释了磷诱导的该激素血清浓度变化。
