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URL Address
<a href="http://doi.org/10.1002/hep.28707" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.28707</a>
Pages
813–827
Issue
3
Volume
65
Dublin Core
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Title
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G-protein-coupled bile acid receptor plays a key role in bile acid metabolism and fasting-induced hepatic steatosis in mice.
Publisher
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Hepatology (Baltimore, Md.)
Date
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2017
2017-03
Subject
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*Gene Expression Regulation; Analysis of Variance; Animal; Animals; Bile Acids and Salts/*metabolism; Disease Models; Energy Metabolism/physiology; Fasting; Fatty Liver/*metabolism/pathology; G-Protein-Coupled/*genetics; Homeostasis/genetics; Inbred C57BL; Lipid Metabolism/genetics; Male; Mice; Oxygen Consumption/physiology; Random Allocation; Receptors; RNA-Binding Proteins/*metabolism; Signal Transduction
Creator
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Donepudi Ajay C; Boehme Shannon; Li Feng; Chiang John Y L
Description
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Bile acids are signaling molecules that play a critical role in regulation of hepatic metabolic homeostasis by activating nuclear farnesoid X receptor (Fxr) and membrane G-protein-coupled receptor (Takeda G-protein-coupled receptor 5; Tgr5). The role of FXR in regulation of bile acid synthesis and hepatic metabolism has been studied extensively. However, the role of TGR5 in hepatic metabolism has not been explored. The liver plays a central role in lipid metabolism, and impaired response to fasting and feeding contributes to steatosis and nonalcoholic fatty liver and obesity. We have performed a detailed analysis of gallbladder bile acid and lipid metabolism in Tgr5(-/-) mice in both free-fed and fasted conditions. Lipid profiles of serum, liver and adipose tissues, bile acid composition, energy metabolism, and messenger RNA and protein expression of the genes involved in lipid metabolism were analyzed. Results showed that deficiency of the Tgr5 gene in mice alleviated fasting-induced hepatic lipid accumulation. Expression of liver oxysterol 7alpha-hydroxylase in the alternative bile acid synthesis pathway was reduced. Analysis of gallbladder bile acid composition showed marked increase of taurocholic acid and decrease of tauro-alpha and beta-muricholic acid in Tgr5(-/-) mice. Tgr5(-/-) mice had increased hepatic fatty acid oxidation rate and decreased hepatic fatty acid uptake. Interestingly, fasting induction of fibroblast growth factor 21 in liver was attenuated. In addition, fasted Tgr5(-/-) mice had increased activation of hepatic growth hormone-signal transducer and activator of transcription 5 (GH-Stat5) signaling compared to wild-type mice. CONCLUSION: TGR5 may play a role in determining bile acid composition and in fasting-induced hepatic steatosis through a novel mechanism involving activation of the GH-Stat5 signaling pathway. (Hepatology 2017;65:813-827).
Identifier
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<a href="http://doi.org/10.1002/hep.28707" target="_blank" rel="noreferrer noopener">10.1002/hep.28707</a>
Rights
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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).
*Gene Expression Regulation
2017
Analysis of Variance
Animal
Animals
Bile Acids and Salts/*metabolism
Boehme Shannon
Chiang John Y L
Department of Integrative Medical Sciences
Disease Models
Donepudi Ajay C
Energy Metabolism/physiology
Fasting
Fatty Liver/*metabolism/pathology
G-Protein-Coupled/*genetics
Hepatology (Baltimore, Md.)
Homeostasis/genetics
Inbred C57BL
Li Feng
Lipid Metabolism/genetics
Male
Mice
NEOMED College of Medicine
Oxygen Consumption/physiology
Random Allocation
Receptors
RNA-Binding Proteins/*metabolism
Signal Transduction