1
40
3
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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.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>
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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).
*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
-
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/10.1159/000497447" target="_blank" rel="noreferrer noopener">http://doi.org/10.1159/000497447</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
1-16
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
Role of Lipoprotein Apheresis in Cardiovascular Disease Risk Reduction.
Publisher
An entity responsible for making the resource available
Blood purification
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
The topic of the resource
Cardiovascular disease; *Atherosclerosis; Lipoprotein apheresis; Lipoprotein(a); Low-density lipoprotein; Peripheral vascular disease
Creator
An entity primarily responsible for making the resource
Raina Rupesh; Young Claire; Krishnappa Vinod; Chanchlani Rahul
Description
An account of the resource
BACKGROUND AND AIM: Elevated low-density lipoprotein cholesterol and/or lipoprotein(a) are established risk factors for cardiovascular disease (CVD). Management of hypercholesterolemia consists of drug therapies, including statins and proprotein convertase subtilisin/kexin type 9 inhibitors. In patients with familial hypercholesterolemia (FH), lipoprotein apheresis (LA) is utilized to control lipid levels. However, LA is not currently a standard therapy for non-FH. This review summarizes the literature regarding LA therapy in CVD prevention. METHODS: PubMed/MEDLINE databases were searched using the keywords "LA" and "CVD". Citations were individually reviewed for relevance. RESULTS: The efficacy of LA was clearly demonstrated, largely based on evidence from observational studies. In patients who are unresponsive to traditional lipid-lowering medications, LA effectively reduced serum lipoprotein levels and adverse cardiovascular events. CONCLUSION: It was concluded that LA is a safe and effective technique that could be considered in the management of hypercholesterolemia and future risk. Randomized control trials would further support a role for LA as a therapeutic option.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1159/000497447" target="_blank" rel="noreferrer noopener">10.1159/000497447</a>
*Atherosclerosis
2019
Blood purification
CARDIOVASCULAR DISEASE
Chanchlani Rahul
Department of Internal Medicine
Krishnappa Vinod
Lipoprotein apheresis
Lipoprotein(a)
Low-density lipoprotein
NEOMED College of Graduate Studies Student
NEOMED College of Medicine
Peripheral vascular disease
Raina Rupesh
Young Claire