Inoue M, Tanaka H, Moriwake T, Oka M, Sekiguchi C, Seino Y
Department of Pediatrics, Okayama University Medical School, Japan.
Bone. 2000 Mar;26(3):281-6. doi: 10.1016/s8756-3282(99)00282-3.
Microgravity induces significant and progressive bone loss in both humans and animals. This is the consequence of disturbed bone remodeling. We performed a bed rest experiment to simulate microgravity and tried to clarify bone metabolism by measuring biochemical markers of bone turnover. Six healthy volunteers participated in 120 days of bed rest. The parameters of calcium homeostasis, calcitropic hormones, and biochemical markers of bone turnover were examined. After ambulatory control evaluation, all subjects underwent 120 days of bed rest. Metabolic evaluation was performed in a baseline period, and on days 7, 16, 50, 72, 92, and 108 during bed rest, and on days 10 and 25 during a recovery period. Bed rest induced an increase in urinary calcium (Ca) excretion and serum Ca and bone resorption markers. Urine pyridinoline, deoxypyridinoline, and type I collagen cross-linked N-telopeptide increased more rapidly than urinary Ca excretion and serum Ca. Tartrate-resistant acid phosphatase (TRAP) increased even in the recovery period. Carboxy-terminal propeptide of type I collagen, a bone formation marker, significantly decreased on days 50, 92, and 108 of bed rest. These changes of biochemical markers of bone metabolism, except for TRAP, rapidly returned toward control levels in the recovery period. Immunoreactive parathyroid hormone showed a modest decrease during bed rest and a significant increase in the recovery period. Insulin-like growth factor I (IGF-I) and its binding protein, insulin-like growth factor binding protein-3, increased during bed rest, indicating the possibility of resistance to IGF-I in bones under reduced mechanical stress and strain. Bone loss from unloading results from the combination of acceleration of bone resorption and subsequent retardation of bone formation.
微重力会导致人类和动物出现显著且渐进性的骨质流失。这是骨重塑紊乱的结果。我们进行了一项卧床休息实验以模拟微重力，并试图通过测量骨转换的生化标志物来阐明骨代谢情况。六名健康志愿者参与了为期120天的卧床休息。对钙稳态参数、促钙激素以及骨转换的生化标志物进行了检测。在进行门诊对照评估后，所有受试者均接受了120天的卧床休息。在基线期、卧床休息期间的第7天、16天、50天、72天、92天和108天以及恢复期的第10天和25天进行了代谢评估。卧床休息导致尿钙（Ca）排泄增加，血清钙和骨吸收标志物升高。尿吡啶啉、脱氧吡啶啉和I型胶原交联N-端肽的增加比尿钙排泄和血清钙更为迅速。即使在恢复期，抗酒石酸酸性磷酸酶（TRAP）仍有所增加。I型胶原羧基末端前肽作为一种骨形成标志物，在卧床休息的第50天、92天和108天显著下降。除TRAP外，这些骨代谢生化标志物的变化在恢复期迅速恢复至对照水平。免疫反应性甲状旁腺激素在卧床休息期间略有下降，而在恢复期显著升高。胰岛素样生长因子I（IGF-I）及其结合蛋白胰岛素样生长因子结合蛋白-3在卧床休息期间升高，这表明在机械应力和应变降低的情况下，骨骼可能存在对IGF-I的抵抗。卸载导致的骨质流失是骨吸收加速和随后骨形成延迟共同作用的结果。
