BEFORE affecting calcium and phosphorus metabolism, vitamin D3 (cholecalciferol) undergoes two hydroxylations; first in the liver, gut and perhaps other organs, to its major circulating form1,2 25(OH)D 3 and then in the kidney3 to 1α,25(OH) 2D3, the hormonal form. 1α,25(OH)2D 3 is the most potent metabolite of cholecalciferol and may be chiefly responsible for all the effects of the vitamin on calcium metabolism 4. Although the regulation of the secretion of 1α,25(OH) 2D3 by the kidney has been a controversial subject, it is generally agreed that 1α,25(OH)2D3 itself 5,6, the calcium and phosphorus content7-9 of the diet and parathyroid hormone (PTH)10 are all involved. But these factors do not seem adequate to account for the increased content of 1α,25(OH) 2D3 in the plasma during growth spurts, pregnancy and lactation11, when the major increases in calcium and phosphorus absorption occur. We thought there might be a clue in the action of prolactin, which strongly increases the secretion of 1α,25(OH)2D 3 in birds12,13 and enhances plasma 1α,25(OH) 2D3 in lactating mammals14. Suppression of prolactin by administration of bromocriptine to lactating rats markedly lowers plasma 1α,25(OH)2D3 levels, although the drug has no such effect in non-lactating controls15. The similarity of the amino acid sequences of prolactin and growth hormone suggested that these hormones might have similar effects. We now report that administration to rats of a highly purified preparation of human growth hormone restores to normal the depressed plasma levels of 1α,25(OH)2D3 produced by hypophysectomy.
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