Increased serum 1,25-dihydroxyvitamin D after growth hormone administration is not parathyroid hormone-mediated.
Increased serum 1,25-dihydroxyvitamin D after growth hormone administration is not parathyroid hormone-mediated.
复制标题
生长激素给药后血清 1,25-二羟基维生素 D 的增加不是甲状旁腺激素介导的。
DOI：
10.1007/s002239900303
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发表时间：
1997
影响因子：
4.2
通讯作者：
Bell,NH
中科院分区：
文献类型：
--
作者：
Wright,NM;Papadea,N;Wentz,B;Hollis,B;Willi,S;Bell,NH
为了评估生长激素 (GH) 对血清 1,25-二羟基维生素 D [1,25(OH)2D] 的影响，我们对六名健康的年轻成年白人男性进行了以下前瞻性交叉研究。在一般临床研究中心两次入院 2.5 天期间，受试者每日膳食钙摄入量为 400 毫克。测量血清钙、磷、1,25(OH)2D、免疫反应性完整甲状旁腺激素 (PTH)、胰岛素样生长因子 I (IGF-I)、IGF 结合蛋白 3 (IGFBP3)、肾小管磷酸盐重吸收 (TRP) 和最大肾小管磷酸盐重吸收 (TMP/GFR)。其中一次入院前和入院期间给予重组人 GH（rhGH，Humatrope）（25 μg/kg/天，皮下注射，持续 1 周）。结果表示为平均值±SEM。而血清 1,25(OH)2D（58.9 ± 7.7 对比 51.6 ± 7.4 pg/ml，P< 0.01）、血清磷（4.5 ± 0.1 对比 3.7 ± 0.1 mg/dl，P< 0.01）、TRP（92.0 ± 0.5 对比 87.8 ± 0.7 mg/dl，P< 0.005）、TMP/GFR（4.6±0.1 vs 3.5±0.2，P<0.005）、尿钙（602±49 vs 346±25 mg/day，P<0.001）显着升高，血清PTH显着降低（19.9±1.9 vs 26.8±4.0 pg/ml，P<0.05）当受试者接受 rhGH 治疗时，血清钙没有变化。这些发现表明，在人类中，GH 独立于循环 PTH 影响血清 1,25(OH)2D，并且这种作用是由 IGF-I 介导的。因此，我们提出，GH 刺激骨量增加的一种潜在机制是通过血清 1,25(OH)2D 的适度增加。
To assess the effects of growth hormone (GH) on serum 1,25-dihydroxyvitamin D [1,25(OH)2D], we performed the following prospective crossover study in six healthy, young, adult, white men. During each of two admissions for 2½ days to a general clinical research center, subjects were placed on a daily dietary calcium intake of 400 mg. Serum calcium, phosphorus, 1,25(OH)2D, immunoreactive intact parathyroid hormone (PTH), insulin-like growth factor I (IGF-I), IGF binding protein 3 (IGFBP3), tubular reabsorption of phosphate (TRP), and maximum tubular reabsorption of phosphate (TMP/GFR) were measured. Recombinant human GH (rhGH, Humatrope) (25 μg/kg/day subcutaneously for 1 week) was administered prior to and during one of the admissions. Results are expressed as mean ± SEM. Whereas serum 1,25(OH)2D (58.9 ± 7.7 versus 51.6 ± 7.4 pg/ml,P< 0.01), serum phosphorus (4.5 ± 0.1 versus 3.7 ± 0.1 mg/dl,P< 0.01), TRP (92.0 ± 0.5 versus 87.8 ± 0.7 mg/dl,P< 0.005), TMP/GFR (4.6 ± 0.1 versus 3.5 ± 0.2,P< 0.005), and urinary calcium (602 ± 49 versus 346 ± 25 mg/day,P< 0.001) increased significantly, serum PTH decreased significantly (19.9 ± 1.9 versus 26.8 ± 4.0 pg/ml,P< 0.05) and serum calcium did not change when subjects received rhGH. These findings indicate that in humans, GH affects serum 1,25(OH)2D independently of circulating PTH and that this effect is mediated by IGF-I. We propose, therefore, that one potential mechanism by which GH stimulates increases in bone mass is via modest increases in serum 1,25(OH)2D.