Premium
FXR‐deficiency confers increased susceptibility to torpor
Author(s) -
Cariou Bertrand,
Bouchaert Emmanuel,
Abdelkarim Mouaadh,
Dumont Julie,
Caron Sandrine,
Fruchart Jean-Charles,
Burcelin Rémy,
Kuipers Folkert,
Staels Bart
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.09.064
Subject(s) - thermogenesis , torpor , endocrinology , medicine , brown adipose tissue , leptin , thermogenin , basal (medicine) , homeostasis , biology , receptor , nuclear receptor , adipose tissue , chemistry , thermoregulation , biochemistry , obesity , gene , insulin , transcription factor
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.