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Molecular Endocrinology 15 (10): 1720-1728
Copyright © 2001 by The Endocrine Society

Farnesoid X-Activated Receptor Induces Apolipoprotein C-II Transcription: a Molecular Mechanism Linking Plasma Triglyceride Levels to Bile Acids

Heidi Rachelle Kast, Catherine M. Nguyen, Christopher J. Sinal, Stacey A. Jones, Bryan A. Laffitte, Karen Reue, Frank J. Gonzalez, Timothy M. Willson and Peter A. Edwards

Departments of Biological Chemistry and Medicine (H.R.K., C.M.N., B.A.L., P.A.E.), University of California, Los Angeles, California 90095; Laboratory of Metabolism (C.J.S., F.J.G.,) Division of Basic Sciences, National Institutes of Health, Bethesda, Maryland 20892; Molecular Biology Institute (K.R., P.A.E.), University of California, Los Angeles, California 90095; GlaxoSmithKline (S.A.J., T.M.W.) Nuclear Receptor Discovery Research, Research Triangle Park, North Carolina 27709

Address all correspondence and requests for reprints to: Peter A. Edwards, Ph.D., Department of Biological Chemistry, University of California, Los Angeles, California 90095. E-mail: pedwards{at}mednet.ucla.edu

The farnesoid X-activated receptor (FXR; NR1H4), a member of the nuclear hormone receptor superfamily, induces gene expression in response to several bile acids, including chenodeoxycholic acid. Here we used suppression subtractive hybridization to identify apolipoprotein C-II (apoC-II) as an FXR target gene. Retroviral expression of FXR in HepG2 cells results in induction of the mRNA encoding apoC-II in response to several FXR ligands. EMSAs demonstrate that recombinant FXR and RXR bind to two FXR response elements that are contained within two important distal enhancer elements (hepatic control regions) that lie 11 kb and 22 kb upstream of the transcription start site of the apoC-II gene. A luciferase reporter gene containing the hepatic control region or two copies of the wild-type FXR response element was activated when FXR-containing cells were treated with FXR ligands. In addition, we report that hepatic expression of both apoC-II and phospholipid transfer protein mRNAs increases when mice are fed diets supplemented with cholic acid, an FXR ligand, and this induction is attenuated in FXR null mice. Finally, we observed decreased plasma triglyceride levels in mice fed cholic acid- containing diets. These results identify a mechanism whereby FXR and its ligands lower plasma triglyceride levels. These findings may have important implications in the clinical management of hyperlipidemias.




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