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Text
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URL Address
<a href="http://doi.org/10.1210/me.2011-1157" target="_blank" rel="noreferrer noopener">http://doi.org/10.1210/me.2011-1157</a>
Pages
272–280
Issue
2
Volume
26
Dublin Core
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Title
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Loss of FXR protects against diet-induced obesity and accelerates liver carcinogenesis in ob/ob mice.
Publisher
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Molecular endocrinology (Baltimore, Md.)
Date
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2012
2012-02
Subject
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Adipose Tissue; Adiposity/genetics; Animals; Brown/pathology; Carcinoma/etiology/*genetics; Cell Transformation; Cytoplasmic and Nuclear/*deficiency/genetics; Diet; Dietary Fats/metabolism; Energy Metabolism/genetics; Female; Gene Knockout Techniques; Glucose Intolerance/complications/genetics; High-Fat/*adverse effects; Intestinal Absorption; Knockout; Leptin/deficiency/genetics; Liver Neoplasms/etiology/*genetics; Liver/pathology; Male; Mice; Muscle; Neoplastic/genetics; Obese; Obesity/*etiology/genetics; Receptors; Sex Factors; Skeletal/metabolism; Weight Gain/genetics
Creator
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Zhang Yanqiao; Ge Xuemei; Heemstra Lydia A; Chen Wei-Dong; Xu Jiesi; Smith Joseph L; Ma Huiyan; Kasim Neda; Edwards Peter A; Novak Colleen M
Description
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Farnesoid X receptor (FXR) is known to play important regulatory roles in bile acid, lipid, and carbohydrate metabolism. Aged (\textgreater12 months old) Fxr(-/-) mice also develop spontaneous liver carcinomas. In this report, we used three mouse models to investigate the role of FXR deficiency in obesity. As compared with low-density lipoprotein receptor (Ldlr) knockout (Ldlr(-/-)) mice, the Ldlr(-/-)Fxr(-/-) double-knockout mice were highly resistant to diet-induced obesity, which was associated with increased expression of genes involved in energy metabolism in the skeletal muscle and brown adipose tissue. Such a striking effect of FXR deficiency on obesity on an Ldlr(-/-) background led us to investigate whether FXR deficiency alone is sufficient to affect obesity. As compared with wild-type mice, Fxr(-/-) mice showed resistance to diet-induced weight gain. Interestingly, only female Fxr(-/-) mice showed significant resistance to diet-induced obesity, which was accompanied by increased energy expenditure in these mice. Finally, we determined the effect of FXR deficiency on obesity in a genetically obese and diabetic mouse model. We generated ob(-/-)Fxr(-/-) mice that were deficient in both Leptin and Fxr. On a chow diet, ob(-/-)Fxr(-/-) mice gained less body weight and had reduced body fat mass as compared with ob/ob mice. In addition, we observed liver carcinomas in 43% of young (\textless11 months old) Ob(-/-)Fxr(-/-) mice. Together these data indicate that loss of FXR prevents diet-induced or genetic obesity and accelerates liver carcinogenesis under diabetic conditions.
Identifier
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<a href="http://doi.org/10.1210/me.2011-1157" target="_blank" rel="noreferrer noopener">10.1210/me.2011-1157</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2012
Adipose Tissue
Adiposity/genetics
Animals
Brown/pathology
Carcinoma/etiology/*genetics
Cell Transformation
Chen Wei-Dong
Cytoplasmic and Nuclear/*deficiency/genetics
Diet
Dietary Fats/metabolism
Edwards Peter A
Energy Metabolism/genetics
Female
Ge Xuemei
Gene Knockout Techniques
Glucose Intolerance/complications/genetics
Heemstra Lydia A
High-Fat/*adverse effects
Intestinal Absorption
Kasim Neda
Knockout
Leptin/deficiency/genetics
Liver Neoplasms/etiology/*genetics
Liver/pathology
Ma Huiyan
Male
Mice
Molecular endocrinology (Baltimore, Md.)
Muscle
Neoplastic/genetics
Novak Colleen M
Obese
Obesity/*etiology/genetics
Receptors
Sex Factors
Skeletal/metabolism
Smith Joseph L
Weight Gain/genetics
Xu Jiesi
Zhang Yanqiao