Archives of Biochemistry and Biophysics vol:460 issue:2 pages:300-305
Reduced intestinal calcium absorption may be part of the pathogenesis of glucocorticoid-induced osteoporosis. 1,25(OH)(2)D(3) is the major regulator of the expression of the active duodenal calcium absorption genes: TRPV6 (influx), calbindin-D(9K) (intracellular transfer) and PMCA(1b) (extrusion). We investigated the influence of dexamethasone (5days: 2mg/kg bw) on calcium absorption in vivo and on the expression of intestinal and renal calcium transporters in calcium-deprived mice. Total and free 1,25(OH)(2)D(3)-concentrations were halved, in line with decreased 25(OH)D(3)-1-alpha-hydroxylase and increased 24-hydroxylase expression. Nevertheless, no difference in duodenal or renal calcium transporter expression pattern could be detected between vehicle and dexamethasone-treated mice. Accordingly, dexamethasone did not affect in vivo calcium absorption. By contrast, increased calcemia and collagen C-terminal telopeptide levels reflected increased bone resorption. Decreased osteocalcin levels suggested impaired bone formation. Hence, short-term glucocorticoid excess in young animals affected bone metabolism without detectable changes in intestinal or renal calcium handling.