The Effect of Prednisolone® upon the Metabolism and Action of 25-Hydroxy and 1,25-Dihydroxyvitamin D ₃

Abstract

(Amersham, England). The animals were killed 7 hr later. The intestinal mucosa, kidneys, bone, and liver were removed and extracted with chloroform-methanol (2:1) by the method of Bligh and Dyer (12). After extraction, the chloroform phase was dried in a rotary evaporator, taken up in a small volume of solvent, and subjected to chromatography on a 1 X 60-cm column of Sephadex LH20. Stepwise elution with chloroform-hexane (65:35), followed by chloroform-hexane (75:25) was used (13). Fractions (2 ml) were collected, dried, and counted in a Intestinal calcium transport was assessed by the evertedloop technique of Schachter and Rosen (9). Vitamin D-deficient rats were divided into two groups: control and Prednisolone®-treated. The Prednisolones was given subcutaneously for 5 days at a dose of 20 mg/kg per day. On the last day, 7 hr before they were killed, appropriate groups

Altered mineral metabolism in glucocorticoid-induced osteopenia. Effect of 25-hydroxyvitamin D administration.

“…This viewpoint is supported by the observations of (a) Carre et al (21) who have suggested that glucocorticoids may accelerate the metabolism of 1,25-(OH)2D3 to an inactive product, and (b) Klein et al (19) who have reported that 1,25-(OH)2D3 in near-physiologic doses can restore intestinal calcium absorption to approximately normal levels in glucocorticoid-treated individuals. On the other hand, it has been reported that conversion of vitamin D3 to 1,25-(OH)2D3 and localization of 1,25-(OH)2D3 in intestinal mucosal cell nuclei proceeds normally in cortisone-treated rats (22).…”

“…Several authors have suggested that glucocorticoids may reduce serum 25-hydroxyvitamin D (25-OHD) concentration either by impairing the hepatic conversion of vitamin D to 25-OHD or by altering subsequent 25-OHD metabolism (19)(20)(21). In contrast, others have reported normal conversion of [3H]vitamin D3 to its active metabolites in cortisone-treated rats (17,22) and normal serum 25-OHD concentrations, measured by competitive-protein binding assay, in steroid-treated patients (23,24).…”

Reversal of prednisolone-induced inhibition of intestinal calcium-binding protein synthesis by 1.ALPHA.-hydroxycholecalciferol in chicks.

“…For all this the relative weight of parathyroid glands decreased, but it remained supernormal. These findings are in accord with the information of the ability of 1,25/OH/2D3, in contrast to 25/OH/D3, to restore the transport of calcium in intestine of prednisolone-treated rats (Carre et al 1974). The ability of la/OH/D3 to induce CaBP biosynthesis in prednisolone-treated animals supports the hypothesis of the physiologic action disturbance of 1,25/OH/2D3 under the effect of pharmacologic doses of glucocorticoids and indicates the intact state of vitamin D3-25-hydroxylase.…”

Regulation of vitamin D-1alpha-hydroxylase and -24-hydroxylase expression by dexamethasone in mouse kidney

“…Moreover, whether chronic glucocorticoid excess influences plasma concentrations of 24,25(OH) 2 D 3 is not known. Clearance rates of 1,25(OH) 2 D 3 have been found to be normal in humans receiving glucocorticoids (Seeman et al 1980), although the steroids accelerate degradation of 1,25(OH) 2 D 3 in intestinal mucosa (Carré et al 1974). Intestinal receptors for 1,25(OH) 2 D 3 have been reported to be increased in rats (Hirst & Feldman 1982a) by glucocorticoids, but decreased in mice (Hirst & Feldman 1982b).…”