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      Fibroblast growth factor 15 functions as an enterohepatic signal to regulate bile acid homeostasis.

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          Abstract

          The liver and intestine play crucial roles in maintaining bile acid homeostasis. Here, we demonstrate that fibroblast growth factor 15 (FGF15) signals from intestine to liver to repress the gene encoding cholesterol 7alpha-hydroxylase (CYP7A1), which catalyzes the first and rate-limiting step in the classical bile acid synthetic pathway. FGF15 expression is stimulated in the small intestine by the nuclear bile acid receptor FXR and represses Cyp7a1 in liver through a mechanism that involves FGF receptor 4 (FGFR4) and the orphan nuclear receptor SHP. Mice lacking FGF15 have increased hepatic CYP7A1 mRNA and protein levels and corresponding increases in CYP7A1 enzyme activity and fecal bile acid excretion. These studies define FGF15 and FGFR4 as components of a gut-liver signaling pathway that synergizes with SHP to regulate bile acid synthesis.

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          Author and article information

          Journal
          Cell Metab
          Cell metabolism
          Elsevier BV
          1550-4131
          1550-4131
          Oct 2005
          : 2
          : 4
          Affiliations
          [1 ] Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
          Article
          S1550-4131(05)00261-5
          10.1016/j.cmet.2005.09.001
          16213224
          edd9012e-08dc-468e-b94e-6cff4f56e313
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