1
40
2
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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/10.1016/j.molmet.2017.08.011" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.molmet.2017.08.011</a>
Rights
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
1517-1528
Issue
11
Volume
6
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Decreasing Cb1 Receptor Signaling In Kupffer Cells Improves Insulin Sensitivity In Obese Mice
Publisher
An entity responsible for making the resource available
Molecular Metabolism
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-11
Subject
The topic of the resource
adiponectin receptors; adipose-tissue; CB1 receptors; disruption; endocannabinoid system; Endocrinology & Metabolism; fatty liver-disease; Inflammation; Insulin resistance; Kupffer cells; macrophage polarization; nf-kappa-b; nonalcoholic steatohepatitis; protein-2; reactive oxygen; siRNA; targeted; uncoupling
Creator
An entity primarily responsible for making the resource
Jourdan T; Nicoloro S M; Zhou Z; Shen Y F; Liu J; Coffey N J; Cinar R; Godlewski G; Gao B; Aouadi M; Czech M P; Kunos G
Description
An account of the resource
Objective: Obesity-induced accumulation of ectopic fat in the liver is thought to contribute to the development of insulin resistance, and increased activity of hepatic CB1R has been shown to promote both processes. However, lipid accumulation in liver can be experimentally dissociated from insulin resistance under certain conditions, suggesting the involvement of additional mechanisms. Obesity is also associated with pro-inflammatory changes which, in turn, can promote insulin resistance. Kupffer cells (KCs), the liver's resident macrophages, are the major source of pro-inflammatory cytokines in the liver, such as TNF-alpha, which has been shown to inhibit insulin signaling in multiple cell types, including hepatocytes. Here, we sought to identify the role of CB1R in KCs in obesity-induced hepatic insulin resistance. Methods: We used intravenously administered beta-D-glucan-encapsulated siRNA to knock-down CB1R gene expression selectively in KCs. Results: We demonstrate that a robust knock-down of the expression of Cnr1, the gene encoding CB1R, results in improved glucose tolerance and insulin sensitivity in diet-induced obese mice, without affecting hepatic lipid content or body weight. Moreover, Cnr1 knock-down in KCs was associated with a shift from pro-inflammatory M1 to anti-inflammatory M2 cytokine profile and improved insulin signaling as reflected by increased insulin-induced Akt phosphorylation. Conclusion: These findings suggest that CB1R expressed in KCs plays a critical role in obesity-related hepatic insulin resistance via a pro inflammatory mechanism. Published by Elsevier GmbH.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.molmet.2017.08.011" target="_blank" rel="noreferrer noopener">10.1016/j.molmet.2017.08.011</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2017
adiponectin receptors
adipose-tissue
Aouadi M
cb1 receptors
Cinar R
Coffey N J
Czech M P
disruption
endocannabinoid system
Endocrinology & Metabolism
fatty liver-disease
Gao B
Godlewski G
Inflammation
Insulin Resistance
Jourdan T
Journal Article or Conference Abstract Publication
Kunos G
Kupffer cells
Liu J
macrophage polarization
Molecular metabolism
nf-kappa-b
Nicoloro S M
Nonalcoholic steatohepatitis
protein-2
Reactive oxygen
Shen Y F
siRNA
targeted
uncoupling
Zhou Z
-
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/10.1371/journal.pone.0068845" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0068845</a>
Rights
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
11-11
Issue
7
Volume
8
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Hepatic Cannabinoid Receptor Type 1 Mediates Alcohol-Induced Regulation of Bile Acid Enzyme Genes Expression Via CREBH
Publisher
An entity responsible for making the resource available
PLOS ONE
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-07
Subject
The topic of the resource
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
An entity primarily responsible for making the resource
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
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0068845" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0068845</a>
Format
The file format, physical medium, or dimensions of the resource
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