FXR-deficiency confers increased susceptibility to torpor

Bertrand Cariou, Emmanuel Bouchaert, Mouaadh Abdelkarim, Julie Dumont, Sandrine Caron, Jean-Charles Fruchart, Remy Burcelin, Folkert Kuipers, Bart Staels*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

22 Citations (Scopus)

Abstract

The role of the nuclear receptor FXR in adaptive thermogenesis was investigated using FXR-deficient mice. Despite elevated serum bile acid concentrations and increased mRNA expression profiles of thermogenic genes in brown adipose tissue, FXR-deficiency did not alter energy expenditure under basal conditions. However, FXR-deficiency accelerated the fasting-induced entry into torpor in a leptin-dependent manner. FXR-deficient mice were also extremely cold-intolerant. These altered responses may be linked to a more rapid decrease in plasma concentrations of metabolic fuels (glucose, triglycerides) thus impairing uncoupling protein 1-driven thermogenesis. These results identify FXR as a modulator of energy homeostasis. (C) 2007 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

Original languageEnglish
Pages (from-to)5191-5198
Number of pages8
JournalFEBS Letters
Volume581
Issue number27
DOIs
Publication statusPublished - 13-Nov-2007

Keywords

  • thermogenesis
  • fasting
  • cold-exposure
  • nuclear receptor
  • FARNESOID-X-RECEPTOR
  • BILE-ACID
  • ADAPTIVE THERMOGENESIS
  • UNCOUPLING PROTEIN
  • MICE
  • EXPRESSION
  • ADIPOSE
  • OBESITY
  • LEPTIN
  • FAT

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