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on July 21, 2005

Arteriosclerosis, Thrombosis, and Vascular Biology. 2005
Published online before print July 21, 2005, doi: 10.1161/01.ATV.0000178994.21828.a7
A more recent version of this article appeared on October 1, 2005
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Submitted on January 6, 2005
Accepted on July 13, 2005

The Farnesoid X Receptor. A Molecular Link Between Bile Acid and Lipid and Glucose Metabolism

Thierry Claudel *; Bart Staels ; and Folkert Kuipers

From the Center for Liver, Digestive, and Metabolic Diseases (T.C., F.K.), Laboratory of Pediatrics, University Medical Center Groningen, the Netherlands; Unité de Recherche 545 (B.S.), INSERM Département d’Athérosclérose, Institut Pasteur de Lille, and the Faculté de Pharmacie, Université de Lille II, Lille, France.

* To whom correspondence should be addressed. E-mail: t.claudel{at}med.rug.nl.

Abstract--Bile acids are the end products of cholesterol metabolism. They are synthesized in the liver and secreted via bile into the intestine, where they aid in the absorption of fat-soluble vitamins and dietary fat. Subsequently, bile acids return to the liver to complete their enterohepatic circulation. The Farnesoid X receptor (FXR) is a member of the nuclear receptor superfamily and has emerged as a key player in the control of multiple metabolic pathways. On its activation by bile acids, FXR regulates bile acid synthesis, conjugation, and transport, as well as various aspects of lipid and glucose metabolism. This review summarizes recent advances in deciphering the role of FXR in the context of hepatic lipid and glucose homeostasis and discusses the potential of FXR as a pharmacological target for therapeutic applications.


Key words: bile acid • FXR • glucose metabolism • lipid • nuclear receptor




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