FXR-deficiency confers increased susceptibility to torpor

被引：31

作者：

Cariou, Bertrand ^{[1
,2
,3
]}

Bouchaert, Emmanuel ^{[1
,2
,3
]}

Abdelkarim, Mouaadh ^{[1
,2
,3
]}

Dumont, Julie ^{[1
,2
,3
]}

Caron, Sandrine ^{[1
,2
,3
]}

Fruchart, Jean-Charles ^{[1
,2
,3
]}

Burcelin, Remy ^{[4
]}

Kuipers, Folkert ^{[5
]}

Staels, Bart ^{[1
,2
,3
]}

机构：

[1] Inst Pasteur, Dept Atherosclerose, F-59019 Lille, France

[2] INSERM, U545, F-59019 Lille, France

[3] Univ Lille 2, Fac Pharm, Fac Med, F-59006 Lille, France

[4] Univ Toulouse 3, Hop Rangueil, IFR 31,, Inst Mol Med,INSERM,U858, F-31432 Toulouse 4, France

[5] Univ Groningen, Univ Med Ctr Groningen, Pediat Lab, Ctr Liver Digest & Metab Dis, NL-9713 AV Groningen, Netherlands

来源：

FEBS LETTERS | 2007年 / 581卷 / 27期

关键词：

thermogenesis; fasting; cold-exposure; nuclear receptor;

D O I：

10.1016/j.febslet.2007.09.064

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：5191 / 5198

页数：8

共 24 条

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