FEBS Letters
Volume 582, Issue 1 , Pages 10-18, 9 January 2008

FXR signaling in metabolic disease

Edited by Peter Tontonoz and Laszlo Nagy

  • Yanqiao Zhang

      Affiliations

    • Department of Biological Chemistry, University of California at Los Angeles, 47-105 CHS, 10833 Le Conte Avenue, Los Angeles, CA 90095, USA
    • Department of Medicine, University of California at Los Angeles, CA 90095, USA
    • Corresponding Author InformationCorresponding author. Address: Department of Medicine, University of California at Los Angeles, BH-307 CHS, 10833 Le Conte Avenue, Los Angeles, CA 90095, USA. Fax: +1 310 794 7345.
  • ,
  • Peter A. Edwards

      Affiliations

    • Department of Biological Chemistry, University of California at Los Angeles, 47-105 CHS, 10833 Le Conte Avenue, Los Angeles, CA 90095, USA
    • Department of Medicine, University of California at Los Angeles, CA 90095, USA
    • The Molecular Biology Institute, University of California at Los Angeles, CA 90095, USA

Received 6 April 2007; accepted 6 November 2007. published online 15 November 2007.

Abstract 

Farnesoid X receptor (FXR), a member of the nuclear receptor superfamily, has been shown to be important in controlling numerous metabolic pathways; these include roles in maintaining bile acid, lipid and glucose homeostasis, in preventing intestinal bacterial infection and gallstone formation and in modulating liver regeneration and tumorigenesis. The accumulating data suggest that FXR may be a pharmaceutical target for the treatment of certain metabolic diseases.

Keywords: FXR, Bile acid, Lipid, Glucose

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

PII: S0014-5793(07)01159-3

doi:10.1016/j.febslet.2007.11.015

FEBS Letters
Volume 582, Issue 1 , Pages 10-18, 9 January 2008