1
40
4
-
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.bbalip.2018.12.012" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.bbalip.2018.12.012</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
358-371
Issue
3
Volume
1864
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
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
Identification of a novel function of hepatic long-chain acyl-CoA synthetase-1 (ACSL1) in bile acid synthesis and its regulation by bile acid-activated farnesoid X receptor.
Publisher
An entity responsible for making the resource available
Biochimica et biophysica acta. Molecular and cell biology of lipids
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-03
Subject
The topic of the resource
ACSL1; Bile acid synthesis; *Farnesoid X receptor; Gene expression profiling; Hypercholesterolemia; Obeticholic acid
Creator
An entity primarily responsible for making the resource
Singh Amar Bahadur; Dong Bin; Xu Yanyong; Zhang Yanqiao; Liu Jingwen
Description
An account of the resource
Long-chain acyl-CoA synthetase 1 (ACSL1) plays a pivotal role in fatty acid betaoxidation in heart, adipose tissue and skeletal muscle. However, key functions of ACSL1 in the liver remain largely unknown. We investigated acute effects of hepatic ACSL1 deficiency on lipid metabolism in adult mice under hyperlipidemic and normolipidemic conditions. We knocked down hepatic ACSL1 expression using adenovirus expressing a ACSL1 shRNA (Ad-shAcsl1) in mice fed a high-fat diet or a normal chow diet. Hepatic ACSL1 depletion generated a hypercholesterolemic phenotype in mice fed both diets with marked elevations of total cholesterol, LDL-cholesterol and free cholesterol in circulation and accumulations of cholesterol in the liver. Furthermore, SREBP2 pathway in ACSL1 depleted livers was severely repressed with a 50% reduction of LDL receptor protein levels. In contrast to the dysregulated cholesterol metabolism, serum triglycerides, free fatty acid and phospholipid levels were unaffected. Mechanistic investigations of genome-wide gene expression profiling and pathway analysis revealed that ACSL1 depletion repressed expressions of several key enzymes for bile acid biosynthesis, consequently leading to reduced liver bile acid levels and altered bile acid compositions. These results are the first demonstration of a requisite role of ACSL1 in bile acid biosynthetic pathway in liver tissue. Furthermore, we discovered that Acsl1 is a novel molecular target of the bile acid-activated farnesoid X receptor (FXR). Activation of FXR by agonist obeticholic acid repressed the expression of ACSL1 protein and mRNA in the liver of FXR wild-type mice but not in FXR knockout mice.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.bbalip.2018.12.012" target="_blank" rel="noreferrer noopener">10.1016/j.bbalip.2018.12.012</a>
*Farnesoid X receptor
2019
ACSL1
Bile acid synthesis
Biochimica et biophysica acta. Molecular and cell biology of lipids
Department of Integrative Medical Sciences
Dong Bin
Gene Expression Profiling
Hypercholesterolemia
Liu Jingwen
NEOMED College of Medicine
Obeticholic acid
Singh Amar Bahadur
Xu Yanyong
Zhang Yanqiao
-
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/10.1194/jlr.M069807" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M069807</a>
Pages
1831–1844
Issue
10
Volume
57
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
Cholesterol 7alpha-hydroxylase protects the liver from inflammation and fibrosis by maintaining cholesterol homeostasis.
Publisher
An entity responsible for making the resource available
Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-10
Subject
The topic of the resource
*bile acid; *Cholesterol 7-alpha-Hydroxylase/genetics/metabolism; *farnesoid X receptor; *Homeostasis; *Liver Cirrhosis/chemically induced/enzymology/genetics/prevention & control; *Liver/enzymology/pathology; *nuclear receptor; *Takeda G protein-coupled receptor 5; Animals; Cholesterol/genetics/*metabolism; G-Protein-Coupled/genetics/metabolism; Hep G2 Cells; Humans; Knockout; Mice; NF-kappa B/genetics/metabolism; Oxidative Stress; Receptors; Tumor Necrosis Factor-alpha/genetics/metabolism
Creator
An entity primarily responsible for making the resource
Liu Hailiang; Pathak Preeti; Boehme Shannon; Chiang John Y L
Description
An account of the resource
Cholesterol 7alpha-hydroxylase (CYP7A1) plays a critical role in control of bile acid and cholesterol homeostasis. Bile acids activate farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5) to regulate lipid, glucose, and energy metabolism. However, the role of bile acids in hepatic inflammation and fibrosis remains unclear. In this study, we showed that adenovirus-mediated overexpression of Cyp7a1 ameliorated lipopolysaccharide (LPS)-induced inflammatory cell infiltration and pro-inflammatory cytokine production in WT and
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M069807" target="_blank" rel="noreferrer noopener">10.1194/jlr.M069807</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).
*bile acid
*Cholesterol 7-alpha-Hydroxylase/genetics/metabolism
*Farnesoid X receptor
*Homeostasis
*Liver Cirrhosis/chemically induced/enzymology/genetics/prevention & control
*Liver/enzymology/pathology
*nuclear receptor
*Takeda G protein-coupled receptor 5
2016
Animals
Boehme Shannon
Chiang John Y L
Cholesterol/genetics/*metabolism
Department of Integrative Medical Sciences
G-Protein-Coupled/genetics/metabolism
Hep G2 Cells
Humans
Journal of lipid research
Knockout
Liu Hailiang
Mice
NEOMED College of Medicine
NF-kappa B/genetics/metabolism
Oxidative Stress
Pathak Preeti
Receptors
Tumor Necrosis Factor-alpha/genetics/metabolism
-
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