Kärkkäinen M, Lamberg-Allardt C
Department of Applied Chemistry and Microbiology, University of Helsinki, Finland.
J Bone Miner Res. 1996 Dec;11(12):1905-12. doi: 10.1002/jbmr.5650111211.
We studied the effects of a single oral phosphate (Pi) dose as well as those of three consecutive oral phosphate doses on calcium and bone metabolism. In the first part of the study (P1 study) 10 female volunteers were given orally 1500 mg of Pi in water, as a single dose, or plain water in randomized order at two different sessions. In the second part of the study (P3 study), 10 female volunteers were given orally 1500 mg of Pi, as three separate 500 mg doses in water, or plain water in randomized order. Calcium and bone metabolism was monitored for 24 h by measuring the concentrations of serum ionized calcium (S-iCa), urinary calcium, serum phosphate (S-P), urinary P, serum intact parathyroid hormone (PTH), serum carboxy-terminal propeptide of type I collagen (PICP), serum osteocalcin (BGP), serum carboxy-terminal telopeptide of type I collagen (ICTP), urine deoxypyridinoline (DPD) and bone-specific alkaline phosphatase activity (B-ALP). The S-P increased (p = 0.00005 and p = 0.0005, in the P1 and P3 studies, respectively), the S-iCa concentration declined significantly only in the P1 study (p = 0.0014), the urinary calcium excretion decreased (p = 0.02 and 0.013, in the P1 and P3 studies, respectively), and the PTH concentration rose (p = 0.0083 and p = 0.014, in the P1 and P3 studies, respectively) during the phosphate experiment as compared with the control session. Of the three markers of bone formation studied, PICP declined in the P1 study (p = 0.04), and B-ALP declined in both parts of the study (p = 0.027, p = 0.026, in the P1 and P3 studies, respectively) after phosphate administration, whereas there was no significant change in BGP in either of the studies. The markers of bone resorption, ICTP and DPD, were unaffected by the phosphate load in both studies. In conclusion, acute ingestion of phosphate leads to an increase in S-P, a decrease in S-iCa, and an increase in intact PTH secretion. Our results indicate that these events may lead to an acute inactivation of the early phases of bone formation. In this setting, there was no indication of enhanced bone resorption despite the increase in PTH secretion, which could be due to the combined effect of phosphate and PTH on bone resorption.
我们研究了单次口服磷酸盐(Pi)剂量以及连续三次口服磷酸盐剂量对钙和骨代谢的影响。在研究的第一部分(P1研究)中,10名女性志愿者在两个不同时段,以随机顺序分别口服溶于水中的1500mg Pi单剂量或纯水。在研究的第二部分(P3研究)中,10名女性志愿者以随机顺序分别口服溶于水中的1500mg Pi(分三次,每次500mg)或纯水。通过测量血清离子钙(S-iCa)、尿钙、血清磷酸盐(S-P)、尿磷、血清完整甲状旁腺激素(PTH)、血清I型胶原羧基末端前肽(PICP)、血清骨钙素(BGP)、血清I型胶原羧基末端端肽(ICTP)、尿脱氧吡啶啉(DPD)和骨特异性碱性磷酸酶活性(B-ALP)的浓度,监测钙和骨代谢24小时。与对照时段相比,在磷酸盐实验期间,S-P升高(P1和P3研究中分别为p = 0.00005和p = 0.0005),仅在P1研究中S-iCa浓度显著下降(p = 0.0014),尿钙排泄减少(P1和P3研究中分别为p = 0.02和0.013),PTH浓度升高(P1和P3研究中分别为p = 0.0083和p = 0.014)。在所研究的三个骨形成标志物中,P1研究中PICP下降(p = 0.04),给药后研究的两个部分中B-ALP均下降(P1和P3研究中分别为p = 0.027,p = 0.026),而两项研究中BGP均无显著变化。两项研究中,骨吸收标志物ICTP和DPD均未受磷酸盐负荷影响。总之,急性摄入磷酸盐导致S-P升高、S-iCa降低以及完整PTH分泌增加。我们的结果表明,这些事件可能导致骨形成早期阶段急性失活。在此情况下,尽管PTH分泌增加,但未显示骨吸收增强,这可能是由于磷酸盐和PTH对骨吸收的联合作用。