Springer Online Journal Archives 1860-2000
Summary Hypophysectomy abolishes the four- to fivefold increase in plasma 1,25(OH)2D levels that normally accompanies dietary phosphate deprivation in rats despite a smaller but significant decrease in plasma phosphate in these animals. This effect appears within 1 week of hypophysectomy and may be the result of a lack of GH, T3, or some other pituitary hormone. In hypothyroid rats (2 weeks after TPTX) not given replacement T3, plasma 1,25(OH)2D levels rose threefold from 148±57 pmol/l to 402±96 pmol/l (mean±SD) after 4 days of dietary phosphate deprivation. However, in hypophysectomized animals given replacement T3 alone, plasma 1,25(OH)2D levels rose fourfold from 82±13 to 333±230 pmol/l after 4 days of phosphate deprivation. In addition, in hypophysectomized animals replaced with GH alone, plasma 1,25(OH)2D levels rose from 243±86 to 525±85 pmol/l during phosphate deprivation. These results would suggest that both GH and T3 must be absent to prevent enhanced renal 1,25(OH)2D synthesis during phosphate deprivation. GH and T3 appear to play a permissive role since plasma levels of these hormones do not increase when intact rats are deprived of phosphate. Furthermore, bioassayable somatomedin levels are also not increased in intact rats during phosphate deprivation as well as plasma levels of prolactin. As observed previously, plasma 1,25(OH)2D levels were inversely correlated to plasma phosphate concentrations (r=0.46,P〈0.025), despite the inclusion of data points for unreplaced hypophysectomized animals who were hypophosphatemic but showed no increase in plasma 1,25(OH)2D. Thus the possibility remains that GH and T3 may exert their effect by permitting the renal 25OHD-1α-hydroxylase to respond to a change in phosphate concentrations during dietary phosphate deprivation, that, in turn, may ultimately increase renal 1,25(OH)2D synthesis and plasma levels of this hormone.
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