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The influence of Vitamin D on serum calcium levels cannot be explained by the effect on intestinal absorption of calcium alone. Rather, some alteration in the distribution of calcium between bone and the circulating fluids must occur, a concept that has received in‐direct experimental support. In the study reported below bone (calvaria from mice) was incubated in vitro until a steady‐state equilibrium for calcium and phosphorus between the bone and the incubating fluid was reached, thus at the end of the incubation simulating the situation in vivo. The concentrations of these ions that bone from animals pre‐treated with Vitamin D maintained in their surrounding fluids were significantly higher than Vitamin D deficient controls demonstrating directly the calcium‐mobilizing effect of the vitamin. Further, Vitamin D increased the passive solubility of the bone mineral and lactate production by bone cells, suggesting modifications of bone cell metabolism. In the absence of Vitamin D, parathyroid hormone had the same effects as reported for the vitamin, indicating that the function of parathyroid hormone is independent of the presence of Vitamin D. Some evidence is presented that in mice deprived of Vitamin D secondary hyperparathyroidism exists.
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Nichols et al. (1963) studied this question.
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