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lüll Prednisolone-induced Ca2+ malabsorption is caused by diminished expression of the epithelial Ca2+ channel TRPV6 Huybers S; Naber TH; Bindels RJ; Hoenderop JGAm J Physiol Gastrointest Liver Physiol 2007[Jan]; 292 (1): G92-7Glucocorticoids, such as prednisolone, are often used in clinic because of their anti-inflammatory and immunosuppressive properties. However, glucocorticoids reduce bone mineral density (BMD) as a side effect. Malabsorption of Ca2+ in the intestine is supposed to play an important role in the etiology of low BMD. To elucidate the mechanism of glucocorticoid-induced Ca2+ malabsorption, the present study investigated the effect of prednisolone on the expression and activity of proteins responsible for active intestinal Ca2+ absorption including the epithelial Ca2+ channel TRPV6, calbindin-D(9K), and the plasma membrane ATPase PMCA1b. Therefore, C57BL/6 mice received 10 mg/kg body wt prednisolone daily by oral gavage for 7 days and were compared with control mice receiving vehicle only. An in vivo 45Ca2+ absorption assay indicated that intestinal Ca2+ absorption was diminished after prednisolone treatment. We showed decreased duodenal TRPV6 and calbindin-D(9K) mRNA and protein abundance in prednisolone-treated compared with control mice, whereas PMCA1b mRNA levels were not altered. Importantly, detailed expression studies demonstrated that in mice these Ca2+ transport proteins are predominantly localized in the first 2 cm of the duodenum. Furthermore, serum Ca2+ and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] concentrations remained unchanged by prednisolone treatment. In conclusion, these data suggest that prednisolone reduces the intestinal Ca2+ absorption capacity through diminished duodenal expression of the active Ca2+ transporters TRPV6 and calbindin-D(9K) independent of systemic 1,25(OH)2D3.|*Intestinal Absorption[MESH]|Animals[MESH]|Calbindins[MESH]|Calcium Channels/drug effects/*genetics[MESH]|Calcium Radioisotopes[MESH]|Calcium/*metabolism[MESH]|Disease Models, Animal[MESH]|Duodenum/physiology/physiopathology[MESH]|Gene Expression Regulation/drug effects[MESH]|Intestinal Mucosa/*physiology/physiopathology[MESH]|Malabsorption Syndromes/*physiopathology[MESH]|Mice[MESH]|Mice, Inbred C57BL[MESH]|Polymerase Chain Reaction[MESH]|Prednisolone/*pharmacology[MESH]|S100 Calcium Binding Protein G/genetics[MESH]|TRPV Cation Channels/drug effects/*genetics[MESH] |