title: Effects of 1,25-dihydroxycholecalciferol on intestinal calcium transport in cortisone-treated rats.
abstract: The administration of glucocorticoids may decrease intestinal calcium absorption in vivo and the active transport of calcium in rat duodenum in vitro. It has been suggested that this apparent "anti-vitamin D-like" effect of steroid hormones may be related to alterations in vitamin D metabolism. In order to test this hypothesis, vitamin D-deficient control and cortisone-treated rats were given an intraperitoneal injection of 5.5 IU of 1,25-dihydroxycholecalciferol (1,25-DHCC), the probable end-organ active vitamin D metabolite in the intestine, and 16 h later studies of duodenal calcium transport were performed in modified Ussing chambers. In the vitamin D-deficient state, cortisone administration was associated with a diminution in J(MS), J(Net), and the flux ratio (J(MS)/J(SM)). While the magnitude of the increases in J(MS) and J(Net) that resulted from 1,25-DHCC treatment were approximately the same in control and cortisone-treated animals, 1,25-DHCC failed to restore these parameters to "normal levels" in the steroid-treated rats. Furthermore, contrary to the results obtained in the saline-treated controls, 1,25-DHCC failed to reduce J(SM) in the duodenum from cortisone-treated rats. The cortisone-related defect in calcium transport was due to alterations in both unidirectional calcium fluxes (decrease in J(MS) and increase in J(SM)), such that the J(Net) and the flux ratio (J(MS)/J(SM)) were only approximately 50% of the levels achieved in vitamin D-deficient control animals repleted with the same dose of 1,25-DHCC. The administration of 1,25-DHCC was accompanied by a marked increase in the serum calcium levels of control rats, but there was no such response in the cortisone-treated group. The results support the concept that under the conditions of these experiments in the rat the apparent antagonism between glucocorticoids and vitamin D may be due to steroid hormone-related alterations in end organ function that are independent of any direct interaction between the hormone and the vitamin and that cannot be reversed by the vitamin.
mesh_terms: D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000097:blood / Q000378:metabolism*; D003348:Cortisone / Q000494:pharmacology*; D004100:Dihydroxycholecalciferols / Q000494:pharmacology; D004386:Duodenum / Q000187:drug effects / Q000378:metabolism; D006887:Hydroxycholecalciferols / Q000494:pharmacology*; D007408:Intestinal Absorption / Q000187:drug effects*; D008274:Magnesium / Q000097:blood; D008297:Male; D010758:Phosphorus / Q000097:blood; D051381:Rats; D014808:Vitamin D Deficiency / Q000378:metabolism
chemical_list: D004100:Dihydroxycholecalciferols; D006887:Hydroxycholecalciferols; D010758:Phosphorus; D008274:Magnesium; D002118:Calcium; D003348:Cortisone