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  • Effects of vitamin D compounds on renal and intestinal Ca2+ transport proteins in 25-hydroxyvitamin D3-1alpha-hydroxylase knockout mice
  • Hoenderop JG; van der Kemp AW; Urben CM; Strugnell SA; Bindels RJ
  • Kidney Int 2004[Sep]; 66 (3): 1082-9
  • BACKGROUND: Vitamin D compounds are used clinically to control secondary hyperparathyroidism (SHPT) due to renal failure. Newer vitamin D compounds retain the suppressive action of 1,25(OH)(2)D(3) on the parathyroid glands and may have less Ca(2+)-mobilizing activity, offering potentially safer therapies. METHODS: This study investigated the effect of a single dose of compound (1,25(OH)(2)D(3), 1,24(OH)(2)D(2), or 1alpha(OH)D(2)) on renal and intestinal Ca(2+) transport proteins, including TRPV5 and TRPV6, and serum Ca(2+), in a novel SHPT model, the 25-OH-D(3)-1alpha-hydroxylase knockout mouse, which lacks endogenous 1,25(OH)(2)D(3) and is severely hypocalcemic. Animals were injected intraperitoneally with compound (100 ng/mouse). RESULTS: Serum levels of 1,25(OH)(2)D(3) and 1,24(OH)(2)D(2) peaked at four hours post-injection (pi), then declined rapidly. 1,25(OH)(2)D(2) generated from 1alpha(OH)D(2) peaked at 12 hours pi and then remained stable. Serum Ca(2+) was increased to near-normal within four hours by 1,25(OH)(2)D(3) and 1,24(OH)(2)D(2), and within 12 hours by 1alpha(OH)D(2). 1,25(OH)(2)D(3) and 1,24(OH)(2)D(2) up-regulated duodenal TRPV5 and TRPV6 mRNA to a similar degree within four hours; mRNA levels decreased by 12 hours after 1,24(OH)(2)D(2) treatment, and by 24 hours after 1,25(OH)(2)D(3) treatment. 1,25(OH)(2)D(3) increased kidney levels of TRPV5, calbindin-D(28K), and calbindin-D(9K) mRNA within four hours; 1,24(OH)(2)D(2) did not change kidney TRPV5 levels and modestly increased calbindin D(9K) by 48 hours. 1alpha(OH)D(2) produced later-onset effects, increasing duodenal TRPV6 and calbindin-D(9K) mRNA levels by 12 hours and TRPV5 by 48 hours. CONCLUSION: In kidney, 1alpha(OH)D(2) increased TRPV5, calbindin-D(28K), and calbindin-D(9K) mRNA levels by 12 hours. This study indicates that Ca(2+) transport proteins, including TRPV5 and TRPV6, are differentially up-regulated by vitamin D compounds.
  • |25-Hydroxyvitamin D3 1-alpha-Hydroxylase/*genetics[MESH]
  • |Animals[MESH]
  • |Biological Transport/drug effects/physiology[MESH]
  • |Calbindins[MESH]
  • |Calcitriol/*pharmacology[MESH]
  • |Calcium Channel Agonists/*pharmacology[MESH]
  • |Calcium Channels/genetics/metabolism[MESH]
  • |Calcium/blood[MESH]
  • |Ergocalciferols/pharmacology[MESH]
  • |Intestinal Mucosa/*metabolism[MESH]
  • |Kidney/*metabolism[MESH]
  • |Mice[MESH]
  • |Mice, Knockout[MESH]
  • |RNA, Messenger/metabolism[MESH]
  • |S100 Calcium Binding Protein G/genetics/metabolism[MESH]
  • |TRPV Cation Channels[MESH]
  • |Up-Regulation/drug effects[MESH]
  • |Vitamin D/metabolism[MESH]





  • *{{pmid15327402}}
    *<b>[http://www.kidney.de/mlpefetch.php?search=15327402 Effects of vitamin D compounds on renal and intestinal Ca2+ transport proteins in 25-hydroxyvitamin D3-1alpha-hydroxylase knockout mice ]</b> Kidney Int 2004; 66(3) ; 1082-9 Hoenderop JG; van der Kemp AW; Urben CM; Strugnell SA; Bindels RJ

        *15327402*

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    Kidney Int

    1082 3.66 2004