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  • Hypervitaminosis D mediates compensatory Ca2+ hyperabsorption in TRPV5 knockout mice
  • Renkema KY; Nijenhuis T; van der Eerden BC; van der Kemp AW; Weinans H; van Leeuwen JP; Bindels RJ; Hoenderop JG
  • J Am Soc Nephrol 2005[Nov]; 16 (11): 3188-95
  • Vitamin D plays an important role in Ca(2+) homeostasis by controlling Ca(2+) (re)absorption in intestine, kidney, and bone. The epithelial Ca(2+) channel TRPV5 mediates the Ca(2+) entry step in active Ca(2+) reabsorption. TRPV5 knockout (TRPV5(-/-)) mice show impaired Ca(2+) reabsorption, hypercalciuria, hypervitaminosis D, and intestinal hyperabsorption of Ca(2+). Moreover, these mice demonstrate upregulation of intestinal TRPV6 and calbindin-D(9K) expression compared with wild-type mice. For addressing the role of the observed hypervitaminosis D in the maintenance of Ca(2+) homeostasis and the regulation of expression levels of the Ca(2+) transport proteins in kidney and intestine, TRPV5/25-hydroxyvitamin-D(3)-1alpha-hydroxylase double knockout (TRPV5(-/-)/1alpha-OHase(-/-)) mice, which show undetectable serum 1,25(OH)(2)D(3) levels, were generated. TRPV5(-/-)/1alpha-OHase(-/-) mice displayed a significant hypocalcemia compared with wild-type mice (1.10 +/- 0.02 and 2.54 +/- 0.01 mM, respectively; P < 0.05). mRNA levels of renal calbindin-D(28K) (7 +/- 2%), calbindin-D(9K) (32 +/- 4%), Na(+)/Ca(2+) exchanger (12 +/- 2%), and intestinal TRPV6 (40 +/- 8%) and calbindin-D(9K) (26 +/- 4%) expression levels were decreased compared with wild-type mice. Hyperparathyroidism and rickets were present in TRPV5(-/-)/1alpha-OHase(-/-) mice, more pronounced than observed in single TRPV5 or 1alpha-OHase knockout mice. It is interesting that a renal Ca(2+) leak, as demonstrated in TRPV5(-/-) mice, persisted in TRPV5(-/-)/1alpha-OHase(-/-) mice, but a compensatory upregulation of intestinal Ca(2+) transporters was abolished. In conclusion, the elevation of serum 1,25(OH)(2)D(3) levels in TRPV5(-/-) mice is responsible for the upregulation of intestinal Ca(2+) transporters and Ca(2+) hyperabsorption. Hypervitaminosis D, therefore, is of crucial importance to maintain normocalcemia in impaired Ca(2+) reabsorption in TRPV5(-/-) mice.
  • |Animals[MESH]
  • |Biological Transport[MESH]
  • |Calcium Channels/*deficiency/genetics/*physiology[MESH]
  • |Calcium/blood/*metabolism/urine[MESH]
  • |Crosses, Genetic[MESH]
  • |Female[MESH]
  • |Homeostasis[MESH]
  • |Kidney/physiology[MESH]
  • |Male[MESH]
  • |Metabolic Diseases/*metabolism[MESH]
  • |Mice[MESH]
  • |Mice, Knockout[MESH]
  • |Polymerase Chain Reaction[MESH]
  • |TRPV Cation Channels/*deficiency/genetics/*physiology[MESH]
  • |Vitamin D/*metabolism[MESH]





  • *{{pmid16148038}}
    *<b>[http://www.kidney.de/mlpefetch.php?search=16148038 Hypervitaminosis D mediates compensatory Ca2+ hyperabsorption in TRPV5 knockout mice ]</b> J Am Soc Nephrol 2005; 16(11) ; 3188-95 Renkema KY; Nijenhuis T; van der Eerden BC; van der Kemp AW; Weinans H; van Leeuwen JP; Bindels RJ; Hoenderop JG

        *16148038*

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    J Am Soc Nephrol

    3188 11.16 2005