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Research ArticleGASTROINTESTINAL, HEPATIC, PULMONARY, AND RENAL

Administration of Ampicillin Elevates Hepatic Primary Bile Acid Synthesis through Suppression of Ileal Fibroblast Growth Factor 15 Expression

Masaaki Miyata, Yuki Takamatsu, Hideaki Kuribayashi and Yasushi Yamazoe
Journal of Pharmacology and Experimental Therapeutics December 2009, 331 (3) 1079-1085; DOI: https://doi.org/10.1124/jpet.109.160093
Masaaki Miyata
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Yuki Takamatsu
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Hideaki Kuribayashi
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Yasushi Yamazoe
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Abstract

Administration of the antibacterial drug ampicillin (ABPC) significantly increased hepatic bile acid concentrations. In the present study, we investigated the mechanisms for the elevation of bile acid levels in ABPC-treated mice. Hepatic microsomal cholesterol 7α-hydroxylation and CYP7A1 mRNA level were increased 2.0-fold in ABPC-treated mice despite higher bile acid levels in the liver and small intestinal lumen. A significant change in hepatic small heterodimer partner (SHP) mRNA level was not observed in ABPC-treated mice, whereas a marked decrease in ileal fibroblast growth factor 15 (FGF15) mRNA level was observed (3% of vehicle-treated mice). These phenomena were also observed in mice cotreated with bacitracin/streptomycin/neomycin, which are barely absorbed from the intestine. Primary bile acid contents in the small intestinal lumen were increased in ABPC-treated mice, whereas secondary bile acid, deoxycholic acid (DCA), contents were reduced to below detection limits (<0.01 μmol). In ABPC-treated mice, cotreatment with tauroDCA reversed reductions in ileal FGF15 mRNA level. Ileal SHP mRNA level was, however, not decreased in ABPC-treated mice. ABPC administration to farnesoid X receptor (Fxr)-null mice also decreased ileal FGF15 mRNA levels and secondary bile acid content in the small intestinal lumen. These results suggest that ABPC administration elevates hepatic primary bile acid synthesis, at least in part, through suppression of ileal FGF15 expression.

Footnotes

  • This work was supported by the Ministry of Education, Culture, Sports Science and Technology of Japan [Grants 21390039, 20590137].

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

    doi:10.1124/jpet.109.160093

  • ABBREVIATIONS:

    ABPC
    ampicillin
    SHP
    small heterodimer partner
    FGF15
    fibroblast growth factor 15
    FXR
    farnesoid X receptor
    DCA
    deoxycholic acid
    CDCA
    chenodeoxycholic acid
    CHAPS
    3-[(3-cholamidopropyl)dimethylammonio]propanesulfonate
    LCA
    lithocholic acid
    TDCA
    taurodeoxycholic acid
    BDL
    bile duct-ligated
    BC
    bacitracin
    NM
    neomycin
    SM
    streptomycin
    CA
    cholic acid
    PON1
    paraoxonase 1
    βMCA
    muricholic acid
    TβMCA
    tauro-β-muricholic acid
    TUDCA
    tauroursodeoxycholic acid
    TCA
    taurocholic acid
    TCDCA
    taurochenodeoxycholic acid
    TLCA
    taurolithocholic acid
    UDCA
    ursodeoxycholic acid
    HPLC
    high-performance liquid chromatography
    PCR
    polymerase chain reaction.

    • Received August 7, 2009.
    • Accepted September 17, 2009.
  • © 2009 by The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 376 (3)
Journal of Pharmacology and Experimental Therapeutics
Vol. 376, Issue 3
1 Mar 2021
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Research ArticleGASTROINTESTINAL, HEPATIC, PULMONARY, AND RENAL

Administration of Ampicillin Elevates Hepatic Primary Bile Acid Synthesis through Suppression of Ileal Fibroblast Growth Factor 15 Expression

Masaaki Miyata, Yuki Takamatsu, Hideaki Kuribayashi and Yasushi Yamazoe
Journal of Pharmacology and Experimental Therapeutics December 1, 2009, 331 (3) 1079-1085; DOI: https://doi.org/10.1124/jpet.109.160093

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Research ArticleGASTROINTESTINAL, HEPATIC, PULMONARY, AND RENAL

Administration of Ampicillin Elevates Hepatic Primary Bile Acid Synthesis through Suppression of Ileal Fibroblast Growth Factor 15 Expression

Masaaki Miyata, Yuki Takamatsu, Hideaki Kuribayashi and Yasushi Yamazoe
Journal of Pharmacology and Experimental Therapeutics December 1, 2009, 331 (3) 1079-1085; DOI: https://doi.org/10.1124/jpet.109.160093
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