Response of Chick Parathyroid Glands to the Vitamin D Metabolites, 1,25-Dihydroxycholecalciferol and 24,25-Dihydroxycholecalciferol

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Abstract
Under conditions of chronic hypocalcemia, e.g. in vitamin D depletion, the parathyroid glands undergo marked hypertrophy and hyperplasia. Seven days of treatment (100 IU/day; 6.5 nmoles) with cholecalciferol (CC) decreased parathyroid gland weight significantly from vitamin D depleted controls while increasing serum Ca from 6.3 to 8.6 mg/100 ml. 1,25-Dihydroxycholecalciferol (1.3 nmoles/day) also increased serum Ca to 8.6, but had no effect on gland weight. Both CC and 1,25-dihydroxycholecalciferol stimulated the production of intestinal calcium binding protein. This same dose of 1,25-dihydroxycholecalciferol in combination with small amounts of 24R,25-dihydroxycholecalciferol was as effective as CC in reducing parathyroid gland weight, but 24R,25-dihydroxycholecalciferol alone had no effect on gland weight or on calcium binding protein synthesis. When chicks received a two- to four-fold larger dose of 1,25-dihydroxycholecalciferol, parathyroid gland weight was significantly reduced relative to vitamin D depleted controls. A time course of the action of CC indicated that 4 days treatment was sufficient for significant parathyroid gland size reduction. Decreases in gland wet weight caused by CC were paralleled by decreases in dry weight, and loss of DNA and protein. It is concluded that parathyroid gland regression, involving loss of cells, occurs within a few days of treatment with vitamin D metabolites and that gland regression does not obligatorily follow an increase in serum Ca. At low doses, 1,25-dihydroxycholecalciferol requires the presence of 24R,25-dihydroxycholecalciferol to cause gland regression (but not intestinal calcium binding protein production), whereas it is effective alone at higher doses. These results suggest that the dihydroxylated vitamin D metabolites may play a role in modulating parathyroid gland as well as intestinal function.