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40
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Text
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URL Address
<a href="http://doi.org/10.1371/journal.pone.0068845" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0068845</a>
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Pages
11-11
Issue
7
Volume
8
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Title
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Hepatic Cannabinoid Receptor Type 1 Mediates Alcohol-Induced Regulation of Bile Acid Enzyme Genes Expression Via CREBH
Publisher
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PLOS ONE
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-07
Subject
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metabolism; Ohio; mice; Signaling; Signal transduction; liver; Homeostasis; transcription factor; Genes; exposure; Acids; er stress; endoplasmic-reticulum stress; Science & Technology - Other Topics; insulin-resistance; cholesterol 7-alpha-hydroxylase; human hepatocytes; Rodents; Bile acids; alcohol; element-binding protein; gene-expression; endocannabinoid system; bound; cb1 receptors; leptin resistance; Liver diseases; Diabetes mellitus; insulin-resistance; insulin; Fatty liver; hepatocytes; Sciences: Comprehensive Works; Alcohols; Bile; activation; Damage prevention; Deregulation; Muridae; Regulatory mechanisms (biology); RNA extraction; Synthesis
Creator
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Chanda D; Kim Y H; Li T; Misra J; Kim D K; Kim J R; Kwon J; Jeong W I; Ahn S H; Park T S; Koo S H; Chiang J Y L; Lee C H; Choi H S
Description
An account of the resource
Bile acids concentration in liver is tightly regulated to prevent cell damage. Previous studies have demonstrated that deregulation of bile acid homeostasis can lead to cholestatic liver disease. Recently, we have shown that ER-bound transcription factor Crebh is a downstream effector of hepatic Cb1r signaling pathway. In this study, we have investigated the effect of alcohol exposure on hepatic bile acid homeostasis and elucidated the mediatory roles of Cb1r and Crebh in this process. We found that alcohol exposure or Cb1r-agonist 2-AG treatment increases hepatic bile acid synthesis and serum ALT, AST levels in vivo alongwith significant increase in Crebh gene expression and activation. Alcohol exposure activated Cb1r, Crebh, and perturbed bile acid homeostasis. Overexpression of Crebh increased the expression of key bile acid synthesis enzyme genes via direct binding of Crebh to their promoters, whereas Cb1r knockout and Crebh-knockdown mice were protected against alcohol-induced perturbation of bile acid homeostasis. Interestingly, insulin treatment protected against Cb1r-mediated Crebh-induced disruption of bile acid homeostasis. Furthermore, Crebh expression and activation was found to be markedly increased in insulin resistance conditions and Crebh knockdown in diabetic mice model (db/db) significantly reversed alcohol-induced disruption of bile acid homeostasis. Overall, our study demonstrates a novel regulatory mechanism of hepatic bile acid metabolism by alcohol via Cb1r-mediated activation of Crebh, and suggests that targeting Crebh can be of therapeutic potential in ameliorating alcohol-induced perturbation of bile acid homeostasis.
Identifier
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<a href="http://doi.org/10.1371/journal.pone.0068845" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0068845</a>
Format
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Journal Article or Conference Abstract Publication
2013
Acids
activation
Ahn S H
Alcohol
Alcohols
Bile
BILE acids
bound
cb1 receptors
Chanda D
Chiang J Y L
Choi H S
cholesterol 7-alpha-hydroxylase
Damage prevention
Deregulation
Diabetes Mellitus
element-binding protein
endocannabinoid system
endoplasmic-reticulum stress
er stress
exposure
Fatty Liver
gene-expression
Genes
hepatocytes
Homeostasis
human hepatocytes
insulin
insulin-resistance
Jeong W I
Journal Article or Conference Abstract Publication
Kim D K
Kim J R
Kim Y H
Koo S H
Kwon J
Lee C H
leptin resistance
Li T
Liver
Liver Diseases
Metabolism
Mice
Misra J
Muridae
Ohio
Park T S
PloS one
Regulatory mechanisms (biology)
RNA extraction
Rodents
Science & Technology - Other Topics
Sciences: Comprehensive Works
Signal Transduction
Signaling
Synthesis
transcription factor