1
40
2
-
Text
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n/a
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Pages
398A-398A
Volume
54
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Dublin Core
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Title
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Nutrient Regulation Of Cyp7a1 Expression Links Bile Acid Synthesis To Maintain Metabolic Homeostasis And Prevent Diabetes And Obesity
Publisher
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Hepatology
Date
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2011
2011-10
Subject
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Gastroenterology & Hepatology
Creator
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Li T G; Boehme S M; Ochoa A; Zhang Y C; Klaassen C D; Chiang J
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n/a
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Journal Article or Conference Abstract Publication
2011
Boehme S M
Chiang J
Gastroenterology & Hepatology
Hepatology
Journal Article or Conference Abstract Publication
Klaassen C D
Li T G
Ochoa A
Zhang Y C
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/hep.25740" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.25740</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).
Pages
1034-1043
Issue
3
Volume
56
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Title
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Mechanism Of Tissue-specific Farnesoid X Receptor In Suppressing The Expression Of Genes In Bile-acid Synthesis In Mice
Publisher
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Hepatology
Date
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2012
2012-09
Subject
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7-alpha-hydroxylase; activation; biosynthesis; cholesterol; feedback-regulation; fxr; Gastroenterology & Hepatology; homeostasis; molecular-basis; orphan nuclear receptor; signal; small heterodimer partner
Creator
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Kong B; Wang L; Chiang J Y L; Zhang Y C; Klaassen C D; Guo G L
Description
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Activation of farnesoid X receptor (Fxr, Nr1h4) is a major mechanism in suppressing bile-acid synthesis by reducing the expression levels of genes encoding key bile-acid synthetic enzymes (e.g., cytochrome P450 [CYP]7A1/Cyp7a1 and CYP8B1/Cyp8b1). FXR-mediated induction of hepatic small heterodimer partner (SHP/Shp, Nr0b2) and intestinal fibroblast growth factor 15 (Fgf15; FGF19 in humans) has been shown to be responsible for this suppression. However, the exact contribution of Shp/Fgf15 to this suppression, and the associated cell-signaling pathway, is unclear. By using novel genetically modified mice, the current study showed that the intestinal Fxr/Fgf15 pathway was critical for suppressing both Cyp7a1 and Cyp8b1 gene expression, but the liver Fxr/Shp pathway was important for suppressing Cyp8b1 gene expression and had a minor role in suppressing Cyp7a1 gene expression. Furthermore, in vivo administration of Fgf15 protein to mice led to a strong activation of extracellular signal-related kinase (ERK) and, to a smaller degree, Jun N-terminal kinase (JNK) in the liver. In addition, deficiency of either the ERK or JNK pathway in mouse livers reduced the basal, but not the Fgf15-mediated, suppression of Cyp7a1 and Cyp8b1 gene expression. However, deficiency of both ERK and JNK pathways prevented Fgf15-mediated suppression of Cyp7a1 and Cyp8b1 gene expression. Conclusion: The current study clearly elucidates the underlying molecular mechanism of hepatic versus intestinal Fxr in regulating the expression of genes critical for bile-acid synthesis and hydrophobicity in the liver. (HEPATOLOGY 2012;56:10341043)
Identifier
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<a href="http://doi.org/10.1002/hep.25740" target="_blank" rel="noreferrer noopener">10.1002/hep.25740</a>
Format
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Journal Article or Conference Abstract Publication
2012
7-alpha-hydroxylase
activation
biosynthesis
Chiang J Y L
Cholesterol
feedback-regulation
FXR
Gastroenterology & Hepatology
Guo G L
Hepatology
Homeostasis
Journal Article or Conference Abstract Publication
Klaassen C D
Kong B
molecular-basis
orphan nuclear receptor
signal
small heterodimer partner
Wang L
Zhang Y C