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Endocrinology, doi:10.1210/en.2007-1655
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Endocrinology Vol. 149, No. 6 3196-3205
Copyright © 2008 by The Endocrine Society

Active Intestinal Calcium Transport in the Absence of Transient Receptor Potential Vanilloid Type 6 and Calbindin-D9k

Bryan S. Benn, Dare Ajibade, Angela Porta, Puneet Dhawan, Matthias Hediger, Ji-Bin Peng, Yi Jiang, Goo Taeg Oh, Eui-Bae Jeung, Liesbet Lieben, Roger Bouillon, Geert Carmeliet and Sylvia Christakos

Department of Biochemistry and Molecular Biology (B.S.B., D.A., A.P., P.D., S.C.), University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, New Jersey 07103; Institute of Biochemistry and Molecular Medicine (M.H.), University of Berne, CH-3012 Berne, Switzerland; Department of Medicine (J.-B.P., Y.J.), University of Alabama, Birmingham, Alabama 35294; Laboratory of Cardiovascular Genomics (G.T.O.), Ewha Woman’s University, Seoul 120-750, Korea; Laboratory of Veterinary Biochemistry and Molecular Biology (E.-B.J.), College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 361-763, Korea; and Laboratory of Experimental Medicine and Endocrinology (L.L., R.B., G.C.), Katholieke Universiteit Leuven, Leuven B-3000, Belgium

Address all correspondence and requests for reprints to: Dr. Sylvia Christakos, Department of Biochemistry and Molecular Biology, UMDNJ-New Jersey Medical School E609, 185 South Orange Avenue, Newark, New Jersey 07103. E-mail: christak{at}umdnj.edu.

To study the role of the epithelial calcium channel transient receptor potential vanilloid type 6 (TRPV6) and the calcium-binding protein calbindin-D9k in intestinal calcium absorption, TRPV6 knockout (KO), calbindin-D9k KO, and TRPV6/calbindin-D9k double-KO (DKO) mice were generated. TRPV6 KO, calbindin-D9k KO, and TRPV6/calbindin-D9k DKO mice have serum calcium levels similar to those of wild-type (WT) mice (~10 mg Ca2+/dl). In the TRPV6 KO and the DKO mice, however, there is a 1.8-fold increase in serum PTH levels (P < 0.05 compared with WT). Active intestinal calcium transport was measured using the everted gut sac method. Under low dietary calcium conditions there was a 4.1-, 2.9-, and 3.9-fold increase in calcium transport in the duodenum of WT, TRPV6 KO, and calbindin-D9k KO mice, respectively (n = 8–22 per group; P > 0.1, WT vs. calbindin-D9k KO, and P < 0.05, WT vs. TRPV6 KO on the low-calcium diet). Duodenal calcium transport was increased 2.1-fold in the TRPV6/calbindin-D9k DKO mice fed the low-calcium diet (P < 0.05, WT vs. DKO). Active calcium transport was not stimulated by low dietary calcium in the ileum of the WT or KO mice. 1,25-Dihydroxyvitamin D3 administration to vitamin D-deficient null mutant and WT mice also resulted in a significant increase in duodenal calcium transport (1.4- to 2.0-fold, P < 0.05 compared with vitamin D-deficient mice). This study provides evidence for the first time using null mutant mice that significant active intestinal calcium transport occurs in the absence of TRPV6 and calbindin-D9k, thus challenging the dogma that TRPV6 and calbindin-D9k are essential for vitamin D-induced active intestinal calcium transport.







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