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Drug Metabolism & Disposition

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Modulation of Bile Acid Metabolism by 1α-Hydroxyvitamin D3 Administration in Mice

Shigeru Nishida, Jun Ozeki and Makoto Makishima
Drug Metabolism and Disposition October 2009, 37 (10) 2037-2044; DOI: https://doi.org/10.1124/dmd.109.027334
Shigeru Nishida
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Jun Ozeki
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Makoto Makishima
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Abstract

The vitamin D receptor (VDR) is a nuclear receptor for the active form of vitamin D3 and mediates regulation of calcium homeostasis. Bile acids, such as lithocholic acid, have been identified as additional endogenous VDR ligands. The in vivo role of VDR in bile acid metabolism has not been elucidated. We investigated potential effects of in vivo VDR activation on bile acid metabolism by feeding mice bile acid-supplemented chow and then treating them with 1α-hydroxyvitamin D3 [1α(OH)D3]. We administered 1α(OH)D3 via gavage to mice fed chow supplemented with 0.4% cholic acid (CA), chenodeoxycholic acid (CDCA), deoxycholic acid (DCA), or lithocholic acid (LCA) and examined liver and plasma bile acid composition with gas chromatography-mass spectrometry analysis. 1α(OH)D3 treatment reduced hepatic bile acids in mice fed CDCA- and DCA-supplemented chow but was less effective in mice fed chow supplemented with LCA or CA. 1α(OH)D3 administration also decreased plasma bile acids in mice fed bile acids, such as DCA. The effect of 1α(OH)D3 administration in decreasing liver bile acid composition was observed in mice under fasting conditions and was associated with increased urinary excretion and increased expression of bile acid transporters, such as renal multidrug resistance-associated protein 4. These findings indicate that pharmacological activation of VDR enhances metabolism of bile acids, especially urinary excretion. The results confirm that VDR acts a regulator of bile acid metabolism in vivo.

  • CA, cholic acid
  • CDCA, chenodeoxycholic acid
  • DCA, deoxycholic acid
  • LCA, lithocholic acid
  • FXR, farnesoid X receptor
  • VDR, vitamin D receptor
  • 1,25(OH)2D3, 1α,25-dihydroxyvitamin D3
  • Asbt, apical sodium-dependent bile acid transporter
  • MRP/Mrp, multidrug resistance-associated protein
  • 1α(OH)D3, 1α-hydroxyvitamin D3
  • HDCA, hyodeoxycholic acid
  • UDCA, ursodeoxycholic acid
  • MCA, muricholic acid
  • GC-MS, gas chromatography-mass spectrometry
  • Ntcp, sodium taurocholate-cotransporting polypeptide
  • Oatp, organic anion transporting polypeptide
  • Bsep, bile salt export pump
  • Ost, organic solute transporter.

Footnotes

  • This work was supported in part by the Ministry of Education, Culture, Sports, Science, and Technology, Japan [Grant-in-Aid for Scientific Research on Priority Areas 18077995]; and by Nihon University [Nihon University Joint Research Grant for 2006].

  • Article, publication date, and citation information can be found at http://dmd.aspetjournals.org.

    • Received February 27, 2009.
    • Accepted June 29, 2009.
  • Copyright © 2009 by The American Society for Pharmacology and Experimental Therapeutics
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Drug Metabolism and Disposition: 37 (10)
Drug Metabolism and Disposition
Vol. 37, Issue 10
October 2009
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Modulation of Bile Acid Metabolism by 1α-Hydroxyvitamin D3 Administration in Mice

Shigeru Nishida, Jun Ozeki and Makoto Makishima
Drug Metabolism and Disposition October 1, 2009, 37 (10) 2037-2044; DOI: https://doi.org/10.1124/dmd.109.027334

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Modulation of Bile Acid Metabolism by 1α-Hydroxyvitamin D3 Administration in Mice

Shigeru Nishida, Jun Ozeki and Makoto Makishima
Drug Metabolism and Disposition October 1, 2009, 37 (10) 2037-2044; DOI: https://doi.org/10.1124/dmd.109.027334
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