The effect of vitamin D on bone in vivo

The linear rate of bone mineral apposition (BMAR) was measured in vitamin D-deficient and vitamin D-sufficient adult rats before and during treatment with either 25-hydroxyvitamin D3 (25OHD3), 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], or 24,25-dihydroxyvitamin D3 [24,25-(OH)2D3]. Dietary vitamin D restriction caused a fall in BMAR which began after 1 week and fell progressively to a value of 35-50% of control values by 4 weeks. The fall in BMAR was related to a fall in the serum concentrations of 25(OH)D3 and 24,25-(OH)2D3, without a fall in the 1,25-(OH)2D3 concentration. Dietary supplementation of the D-deficient animals with either 25OHD3 or 24,25-(OH)2D3 at doses of 200 ng/day restored BMAR. If vitamin D-deficient animals were thyroparathyroid-ectomized before supplementation with vitamin D metabolites, 24,25-(OH)2D3 administration was without effect on BMAR. The combined administration of PTH and 24,25-(OH)2D3 to such animals led to a restoration of the BMAR to normal. In vitamin D-sufficient animals, parathyroidectomy led to a 50% reduction in BMAR, which could be restored by treatment with PTH alone but not with 24,25-(OH)2D3. Simultaneous treatment of these animals with PTH and 24,25-(OH)2D3 led to a greater than normal increase in BMAR (130% of control) in these animals. These data support the concept that 24,25-(OH)2D3 has a role in the regulation of bone formation and/or mineralization, and demonstrate the interrelation between the effects of PTH and 24,25-(OH)2D3 on bone.