Effect of growth hormone on vitamin D metabolism

Abstract

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 form^1,2 25(OH)D₃ and then in the kidney³ to 1α,25(OH)₂D₃, the hormonal form. 1α,25(OH)₂D₃ is the most potent metabolite of cholecalciferol and may be chiefly responsible for all the effects of the vitamin on calcium metabolism⁴. 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 content^7–9 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)₂D₃ in birds^12,13 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.