The biological role of 24R, 25(OH)
2D
3 is still controversial, although 24R, 25(OH)
2D
3 has been reported to have peculiar effects particularly on the bone. To examine the biological effects of 24R, 25(OH)
2D
3 we administered Hyp mouse, which is a model for familial X-linked hypophosphatemic rickets in man, 1-10000μg/kg/day of 24R, 25(OH)
2D
3 or 0.01-10μg/kg/day of 1α, 25(OH)
2D
3 for 28 successive days by intraperitoneal injection.
24R, 25(OH)
2D
3 increased the body weight gain, bone size, bone formation and mineralization and reduced the serum alkaline-phosphatase activity, dose-dependently from 1 to 1000μg/kg/day without hypercalcemia.
Severe bone resorption and hypercalcemia were caused by 1 and 10μg/kg/day of 1α, 25(OH)
2D
3, which are considered to be equivalent to 1000μg/kg/day of 24R, 25(OH)
2D
3 in the affinity to the receptor of 1α, 25(OH)
2D
3. On the other hand, 0.1μg/kg/day of 1α, 25(OH)
2D
3 increased bone size, bone formation and mineralization to a similar degree as 1000μg/kg/day of 24R, 25(OH)
2D
3, but did not increase body weight gain, dry bone weight or bone mineral contents, did not reduce serum alkaline-phosphatase activity. At 0.1μg/kg/day, 1α, 25(OH)
2D
3 increased not only bone formation and mineralization but also bone resorption on Hyp mice.
These findings suggest that 24R, 25(OH)
2D
3 has peculiar biological effects on Hyp mouse rather than merely mimicking that of 1α, 25(OH)
2D
3 mediated by its receptor.
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