Springer Online Journal Archives 1860-2000
Summary The mechanism by which dietary phosphate deprivation elevates plasma 1,25-(OH)2-D levels is not known. To evaluate the role of the pituitary in regulating plasma 1,25-(OH)2-D concentrations, the responses of plasma 1,25-(OH)2-D to dietary phosphate deprivation and, separately, to dietary calcium deprivation were evaluated in intact and hypophysectomized male rats. Among intact and hypophysectomized rats eating normal diets, plasma 1,25-(OH)2-D levels averaged 228±76 and 148±62 pmol/1, respectively (P〈0.01). During dietary phosphate deprivation, plasma 1,25-(OH)2-D levels rose to 1160±260 in intact rats and fell to 90±26 pmol/l in hypophysectomized rats (P〈0.001). By contrast, during dietary calcium deprivation, plasma 1,25-(OH)2-D levels rose in both intact and hypophysectomized animals to 856±107 and 742±279 pmol/l, respectively (NS). In response to dietary phosphate deprivation, serum calcium concentrations rose as 1,25-(OH)2-D concentrations rose in intact rats but remained at control levels in hypophysectomized rats. These results support the hypothesis that a pituitary hormone acting either directly or indirectly on the kidney mediates the increase in plasma 1,25-(OH)2-D during dietary phosphate deprivation. The hypercalcemia that occurs in rats during dietary phosphate deprivation appears to depend on the elevation of plasma 1,25-(OH)2-D.
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