1
40
4
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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.2021.101244" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.molmet.2021.101244</a>
Pages
3-11
ISSN
2212-8778
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.molmet.2021.101244" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.molmet.2021.101244</a>
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Update Year & Number
May 2021 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
NEOMED Postdoc Publications
NEOMED Student Publications
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
Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease.
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
2021
2021-04-27
Subject
The topic of the resource
miR-34a; NAFLD; Lipogenesis; bile acids; Bile acids; lipid absorption; lipogenesis; Lipid absorption
Creator
An entity primarily responsible for making the resource
Xu Y; Zhu Y; Hu S; Pan X; Bawa FC; Wang HH; Wang DQ; Yin L; Zhang Y
Description
An account of the resource
Objectives: Hepatic miR-34a expression is elevated in diet-induced or genetically obese mice, and patients with non-alcoholic steatohepatitis (NASH), yet the role of hepatocyte miR-34a in the progression of non-alcoholic fatty liver disease (NAFLD) from non-alcoholic fatty liver (NAFL) to NASH remains to be elucidated.; Methods: Mice over-expressing or deficient in hepatocyte miR-34a and their control mice were fed a diet enriched in fats, cholesterol and fructose (HFCF) to induce NASH. C57BL/6 mice with NASH were treated with an miR-34a inhibitor or a scramble control oligo. The effect of miR-34a on the development, progression or reversal of NAFLD was determined.; Results: Hepatocyte-specific expression of miR-34a aggravated HFCF diet-induced NAFLD. In contrast, germline or adult-onset loss of hepatocyte miR-34a attenuated the development and progression of NAFLD. In addition, pharmacological inhibition of miR-34a reversed HFCF diet-induced steatohepatitis. Mechanistically, hepatocyte miR-34a regulated the development and progression of NAFLD by inducing lipid absorption, lipogenesis, inflammation and apoptosis, and inhibiting fatty acid oxidation.; Conclusions: Hepatocyte miR-34a is an important regulator in the development and progression of NAFLD. MiR-34a may be a useful target for treating NAFLD. (Copyright © 2021 The Author(s). Published by Elsevier GmbH.. All rights reserved.)
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.molmet.2021.101244" target="_blank" rel="noreferrer noopener">10.1016/j.molmet.2021.101244</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).
Format
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journalArticle
2021
Bawa FC
BILE acids
Department of Integrative Medical Sciences
Hu S
journalArticle
lipid absorption
Lipogenesis
May 2021 List
miR-34a
Molecular metabolism
NAFLD
NEOMED College of Medicine
NEOMED Postdoc Publications
NEOMED Student Publications
Pan X
Wang DQ
Wang HH
Xu Y
Yin L
Zhang Y
Zhu Y
-
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
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
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/10.1016/j.molmet.2018.01.005" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.molmet.2018.01.005</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
131-140
Volume
9
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
Reversal of metabolic disorders by pharmacological activation of bile acid receptors TGR5 and FXR.
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
2018
2018-03
Subject
The topic of the resource
Humans; Male; Animals; Mice; *Atherosclerosis; *Farnesoid X receptor; *NAFLD; *Obesity; *TGR5; Diet; Hep G2 Cells; Receptors; Inbred C57BL; High-Fat/adverse effects; Cytoplasmic and Nuclear/*agonists; Bile Acids and Salts/pharmacology/*therapeutic use; Hypercholesterolemia/*drug therapy/etiology/metabolism; Non-alcoholic Fatty Liver Disease/*drug therapy/etiology/metabolism; Obesity/*drug therapy/etiology/metabolism; G-Protein-Coupled/*agonists
Creator
An entity primarily responsible for making the resource
Jadhav Kavita; Xu Yang; Xu Yanyong; Li Yuanyuan; Xu Jiesi; Zhu Yingdong; Adorini Luciano; Lee Yoon Kwang; Kasumov Takhar; Yin Liya; Zhang Yanqiao
Description
An account of the resource
OBJECTIVES: Activation of the bile acid (BA) receptors farnesoid X receptor (FXR) or G protein-coupled bile acid receptor (GPBAR1; TGR5) improves metabolic homeostasis. In this study, we aim to determine the impact of pharmacological activation of bile acid receptors by INT-767 on reversal of diet-induced metabolic disorders, and the relative contribution of FXR vs. TGR5 to INT-767's effects on metabolic parameters. METHODS: Wild-type (WT), Tgr5(-/-), Fxr(-/-), Apoe(-/-) and Shp(-/-) mice were used to investigate whether and how BA receptor activation by INT-767, a semisynthetic agonist for both FXR and TGR5, could reverse diet-induced metabolic disorders. RESULTS: INT-767 reversed HFD-induced obesity dependent on activation of both TGR5 and FXR and also reversed the development of atherosclerosis and non-alcoholic fatty liver disease (NAFLD). Mechanistically, INT-767 improved hypercholesterolemia by activation of FXR and induced thermogenic genes via activation of TGR5 and/or FXR. Furthermore, INT-767 inhibited several lipogenic genes and de novo lipogenesis in the liver via activation of FXR. We identified peroxisome proliferation-activated receptor gamma (PPARgamma) and CCAAT/enhancer-binding protein alpha (CEBPalpha) as novel
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.molmet.2018.01.005" target="_blank" rel="noreferrer noopener">10.1016/j.molmet.2018.01.005</a>
*Atherosclerosis
*Farnesoid X receptor
*NAFLD
*Obesity
*TGR5
2018
Adorini Luciano
Animals
Bile Acids and Salts/pharmacology/*therapeutic use
Cytoplasmic and Nuclear/*agonists
Department of Integrative Medical Sciences
Department of Pharmaceutical Sciences
Diet
G-Protein-Coupled/*agonists
Hep G2 Cells
High-Fat/adverse effects
Humans
Hypercholesterolemia/*drug therapy/etiology/metabolism
Inbred C57BL
Jadhav Kavita
Kasumov Takhar
Lee Yoon Kwang
Li Yuanyuan
Male
Mice
Molecular metabolism
NEOMED College of Medicine
NEOMED College of Pharmacy
Non-alcoholic Fatty Liver Disease/*drug therapy/etiology/metabolism
Obesity/*drug therapy/etiology/metabolism
Receptors
Xu Jiesi
Xu Yang
Xu Yanyong
Yin Liya
Zhang Yanqiao
Zhu Yingdong
-
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.2018.01.005" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.molmet.2018.01.005</a>
Pages
131–140
Volume
9
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
Reversal of metabolic disorders by pharmacological activation of bile acid receptors TGR5 and FXR.
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
2018
2018-03
Subject
The topic of the resource
*Atherosclerosis; *Farnesoid X receptor; *NAFLD; *Obesity; *TGR5
Creator
An entity primarily responsible for making the resource
Jadhav Kavita; Xu Yang; Xu Yanyong; Li Yuanyuan; Xu Jiesi; Zhu Yingdong; Adorini Luciano; Lee Yoon-Kwang; Kasumov Takhar; Yin Liya; Zhang Yanqiao
Description
An account of the resource
OBJECTIVES: Activation of the bile acid (BA) receptors farnesoid X receptor (FXR) or G protein-coupled bile acid receptor (GPBAR1; TGR5) improves metabolic homeostasis. In this study, we aim to determine the impact of pharmacological activation of bile acid receptors by INT-767 on reversal of diet-induced metabolic disorders, and the relative contribution of FXR vs. TGR5 to INT-767's effects on metabolic parameters. METHODS: Wild-type (WT), Tgr5(-/-), Fxr(-/-), Apoe(-/-) and Shp(-/-) mice were used to investigate whether and how BA receptor activation by INT-767, a semisynthetic agonist for both FXR and TGR5, could reverse diet-induced metabolic disorders. RESULTS: INT-767 reversed HFD-induced obesity dependent on activation of both TGR5 and FXR and also reversed the development of atherosclerosis and non-alcoholic fatty liver disease (NAFLD). Mechanistically, INT-767 improved hypercholesterolemia by activation of FXR and induced thermogenic genes via activation of TGR5 and/or FXR. Furthermore, INT-767 inhibited several lipogenic genes and de novo lipogenesis in the liver via activation of FXR. We identified peroxisome proliferation-activated receptor gamma (PPARgamma) and CCAAT/enhancer-binding protein alpha (CEBPalpha) as novel
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.molmet.2018.01.005" target="_blank" rel="noreferrer noopener">10.1016/j.molmet.2018.01.005</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Atherosclerosis
*Farnesoid X receptor
*NAFLD
*Obesity
*TGR5
2018
Adorini Luciano
Department of Integrative Medical Sciences
Department of Pharmaceutical Sciences
Jadhav Kavita
Kasumov Takhar
Lee Yoon-Kwang
Li Yuanyuan
Molecular metabolism
NEOMED College of Medicine
NEOMED College of Pharmacy
Xu Jiesi
Xu Yang
Xu Yanyong
Yin Liya
Zhang Yanqiao
Zhu Yingdong