Hoshino H, Kushida K, Takahashi M, Koyama S, Yamauchi H, Inoue T
Department of Orthopedic Surgery, Hamamatsu University School of Medicine, Japan.
Ann Nutr Metab. 1998;42(2):110-8. doi: 10.1159/000012724.
We have investigated the changes in biochemical markers and in pyridinium cross-links in bone in hypophosphatemic rats. Six-week-old female Wistar rats were divided into two groups (normal diet and a phosphate-deficient diet) and fed for 8 weeks. A low phosphate intake caused a significant difference in the concentrations of osteocalcin and alkaline phosphatase with advancing rachitis as well as an increase in bone resorption marker concentrations in urine. Femur biochemical analysis revealed a significant (p < 0.005) increase in deoxypyridinoline per mole collagen in the phosphate-deficient group which suggested that urinary excretions of pyridinium cross-links might reflect not only bone resorption but also increased pyridinium cross-links in bone matrix collagen. Our results demonstrate that a low phosphate intake causes an increase of pyridinium cross-link formation as well as a discrepancy between the circulation levels of alkaline phosphatase and osteocalcin with advancing rachitis. These alterations induced by low phosphate intake should be considered when interpreting the values of biochemical markers.
我们研究了低磷血症大鼠骨骼中生化标志物和吡啶交联的变化。六周龄雌性Wistar大鼠分为两组（正常饮食组和缺磷饮食组），喂养8周。低磷摄入导致随着佝偻病进展，骨钙素和碱性磷酸酶浓度出现显著差异，同时尿中骨吸收标志物浓度增加。股骨生化分析显示，缺磷组每摩尔胶原蛋白中的脱氧吡啶啉显著增加（p < 0.005），这表明吡啶交联的尿排泄可能不仅反映骨吸收，还反映骨基质胶原蛋白中吡啶交联的增加。我们的结果表明，低磷摄入会导致吡啶交联形成增加，以及随着佝偻病进展，碱性磷酸酶和骨钙素的循环水平出现差异。在解释生化标志物的值时，应考虑低磷摄入引起的这些改变。
