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Duodenal calcium absorption in dexamethasone-treated mice: functional and molecular aspects.

Van Cromphaut SJ, Stockmans I, Torrekens S, Van Herck E, Carmeliet G, Bouillon R

Laboratory of Experimental Medicine and Endocrinology (Legendo), Katholieke Universiteit Leuven, Herestraat 49, Leuven B-3000, Belgium.

Reduced intestinal calcium absorption may be part of the pathogenesis of glucocorticoid-induced osteoporosis. 1,25(OH)2D3 is the major regulator of the expression of the active duodenal calcium absorption genes: TRPV6 (influx), calbindin-D9K (intracellular transfer) and PMCA1b (extrusion). We investigated the influence of dexamethasone (5 days: 2 mg/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)2D3-concentrations were halved, in line with decreased 25(OH)D3-1-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.

Published 23 April 2007 in Arch Biochem Biophys, 460(2): 300-5.
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