Klein L
Proc Natl Acad Sci U S A. 1980 Apr;77(4):1818-22. doi: 10.1073/pnas.77.4.1818.
When bone is remodeled during the growth of a given size bone to a larger size, some bone is resorbed and some is deposited. Much of the resorbed bone mineral, calcium, can be reutilized during bone formation. The net and absolute effects of normal growth, vitamin D deficiency, or vitamin D excess were compared on bone resorption, bone formation, and calcium reutilization. Growing chicks were prelabeled extensively with three isotopes: (45)Ca, [(3)H]tetracycline, and [(3)H]proline. Data were obtained weekly during 3 weeks of control growth, vitamin D deficiency, or vitamin D overdosage while on a nonradioactive diet. Bone resorption as measured by increases in the marrow (inner) diameter of the midshaft of the femur and humerus and by the weekly losses of total [(3)H]tetracycline and [(3)H]collagen per whole bone was not significantly different among any of the groups studied. The data indicated that the high rate of cortical bone resorption in experimental chicks was not increased above that observed in experimental chicks was not increased above that observed in control chicks. Vitamin D deficiency had little effect on the total (45)Ca in whole bones, whereas vitamin D-treated chicks lost 40% of their (45)Ca. Thus, vitamin D overdosage resulted in a decrease of (45)Ca reutilization, whereas vitamin D deficiency resulted in an apparent increase of (45)Ca reutilization. Both vitamin D-deficient and vitamin D-treated chicks had a decreased accumulation of dietary calcium per whole bone. The insufficient mineral mass in vitamin D-deficient chicks resulted from the indirect inhibition of bone mineralization due to the low intestinal absorption of calcium rather than from a change in bone resorption. In vitamin D-treated chicks the apparent bone atrophy and net loss of (45)Ca from bone resulted from inhibiting bone matrix formation and mineralization instead of increasing bone resorption. The constancy of bone resorption under these experimental conditions suggests that bone mineralization is the major regulator of bone mass.
当特定大小的骨骼生长至更大尺寸时进行重塑,一些骨会被吸收,一些则会沉积。大部分被吸收的骨矿物质钙可在骨形成过程中被重新利用。比较了正常生长、维生素D缺乏或维生素D过量对骨吸收、骨形成和钙再利用的净效应和绝对效应。给生长中的雏鸡大量预先标记三种同位素:(45)Ca、[(3)H]四环素和[(3)H]脯氨酸。在对照生长、维生素D缺乏或维生素D过量的3周期间,每周在非放射性饮食条件下获取数据。通过股骨和肱骨中轴骨髓(内侧)直径的增加以及每根全骨每周总[(3)H]四环素和[(3)H]胶原蛋白的损失来测量的骨吸收,在任何研究组之间均无显著差异。数据表明,实验雏鸡皮质骨的高吸收率并未高于对照雏鸡。维生素D缺乏对全骨中的总(45)Ca影响很小,而经维生素D处理的雏鸡损失了其45%的(45)Ca。因此,维生素D过量导致(45)Ca再利用率降低,而维生素D缺乏导致(45)Ca再利用率明显增加。维生素D缺乏和经维生素D处理的雏鸡每根全骨的膳食钙积累均减少。维生素D缺乏雏鸡的矿物质质量不足是由于钙肠道吸收低间接抑制骨矿化所致,而非骨吸收的改变。在经维生素D处理的雏鸡中,明显的骨萎缩和骨中(45)Ca的净损失是由于抑制骨基质形成和矿化,而非增加骨吸收。这些实验条件下骨吸收的恒定表明骨矿化是骨量的主要调节因子。