RapamycinFungusV1, Main, Exploration, bibRecord, 000298

Liraglutide Inhibits Hepatitis C Virus Replication Through an AMP Activated Protein Kinase Dependent Mechanism.

Identifieur interne : 000298 ( Main/Exploration ); précédent : 000297; suivant : 000299

Liraglutide Inhibits Hepatitis C Virus Replication Through an AMP Activated Protein Kinase Dependent Mechanism.

Auteurs : Mei-Yueh Lee [Taïwan] ; Wei-Chun Chen [Taïwan] ; Wei-Hao Hsu [Taïwan] ; Szu-Chia Chen [Taïwan] ; Jin-Ching Lee [Taïwan]

Source :

International journal of molecular sciences [ 1422-0067 ] ; 2019.

RBID : pubmed:31540136

Descripteurs français

KwdFr :
- AMP-Activated Protein Kinases (antagonistes et inhibiteurs), AMP-Activated Protein Kinases (métabolisme), Complexe-2 cible mécanistique de la rapamycine (métabolisme), Glucagon-like peptide 1 (agonistes), Glucagon-like peptide 1 (pharmacologie), Hepacivirus (effets des médicaments et des substances chimiques), Hepacivirus (physiologie), Humains (MeSH), Hépatocytes (enzymologie), Hépatocytes (métabolisme), Hépatocytes (virologie), Lignée cellulaire tumorale (MeSH), Liraglutide (pharmacologie), Phosphoenolpyruvate carboxykinase (ATP) (métabolisme), Phosphorylation (effets des médicaments et des substances chimiques), Récepteur du peptide-1 similaire au glucagon (agonistes), Récepteur du peptide-1 similaire au glucagon (métabolisme), Réplication virale (effets des médicaments et des substances chimiques), Survie cellulaire (effets des médicaments et des substances chimiques), Transduction du signal (effets des médicaments et des substances chimiques).
MESH :
- agonistes : Glucagon-like peptide 1, Récepteur du peptide-1 similaire au glucagon.
- antagonistes et inhibiteurs : AMP-Activated Protein Kinases.
- effets des médicaments et des substances chimiques : Hepacivirus, Phosphorylation, Réplication virale, Survie cellulaire, Transduction du signal.
- enzymologie : Hépatocytes.
- métabolisme : AMP-Activated Protein Kinases, Complexe-2 cible mécanistique de la rapamycine, Hépatocytes, Phosphoenolpyruvate carboxykinase (ATP), Récepteur du peptide-1 similaire au glucagon.
- pharmacologie : Glucagon-like peptide 1, Liraglutide.
- physiologie : Hepacivirus.
- virologie : Hépatocytes.
- Humains, Lignée cellulaire tumorale.

English descriptors

KwdEn :
- AMP-Activated Protein Kinases (antagonists & inhibitors), AMP-Activated Protein Kinases (metabolism), Cell Line, Tumor (MeSH), Cell Survival (drug effects), Glucagon-Like Peptide 1 (agonists), Glucagon-Like Peptide 1 (pharmacology), Glucagon-Like Peptide-1 Receptor (agonists), Glucagon-Like Peptide-1 Receptor (metabolism), Hepacivirus (drug effects), Hepacivirus (physiology), Hepatocytes (enzymology), Hepatocytes (metabolism), Hepatocytes (virology), Humans (MeSH), Liraglutide (pharmacology), Mechanistic Target of Rapamycin Complex 2 (metabolism), Phosphoenolpyruvate Carboxykinase (ATP) (metabolism), Phosphorylation (drug effects), Signal Transduction (drug effects), Virus Replication (drug effects).
MESH :
- chemical , agonists : Glucagon-Like Peptide 1, Glucagon-Like Peptide-1 Receptor.
- chemical , antagonists & inhibitors : AMP-Activated Protein Kinases.
- chemical , metabolism : AMP-Activated Protein Kinases, Glucagon-Like Peptide-1 Receptor, Mechanistic Target of Rapamycin Complex 2, Phosphoenolpyruvate Carboxykinase (ATP).
- drug effects : Cell Survival, Hepacivirus, Phosphorylation, Signal Transduction, Virus Replication.
- enzymology : Hepatocytes.
- metabolism : Hepatocytes.
- chemical , pharmacology : Glucagon-Like Peptide 1, Liraglutide.
- physiology : Hepacivirus.
- virology : Hepatocytes.
- Cell Line, Tumor, Humans.

Abstract

Insulin resistance and diabetes are both associated with chronic hepatitis C virus (HCV) infection, and the glucagon-like peptide-1(GLP-1) receptor agonist, liraglutide, is a common therapy for diabetes. Our aim was to investigate whether liraglutide treatment can inhibit HCV replication. A cell culture-produced HCV infectious system was generated by transfection of in vitro-transcribed genomic JFH-1 ribonucleic acid (RNA) into Huh-7.5 cells. Total RNA samples were extracted to determine the efficiency of HCV replication. The Ava5 cells were treated with liraglutide and cell viability was calculated. A Western blot analysis of the protein expression was performed. The immunoreactive blot signals were also detected. Liraglutide activated GLP-1 receptors in the HCV infectious system, and inhibited subgenomic HCV RNA replication in the HuH-7.5 cells. The Western blot analysis revealed both HCV protein and replicon RNA were reduced after treatment with liraglutide in a dose-dependent manner. Liraglutide decreased the cell viability of HCV RNA at an optimum concentration of 120 μg/mL, activated the 5' adenosine monophosphate-activated protein kinase (AMPK) and the phosphorylated- transducer of regulated cyclic adenosine monophosphate (CAMP) response element-binding protein 2 (TORC2), thereby decreasing the cell viability of phosphoenolpyruvate carboxykinase (PEPCK) and G6pase RNA Therefore, we conclude that liraglutide can inhibit HCV replication via an AMPK/TORC2-dependent pathway.

DOI: 10.3390/ijms20184569
PubMed: 31540136
PubMed Central: PMC6769880

Affiliations:

Taïwan

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000192
to stream Main, to step Curation: 000192

Le document en format XML

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<term>Glucagon-Like Peptide 1 (agonists)</term>
<term>Glucagon-Like Peptide 1 (pharmacology)</term>
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<term>Hepatocytes (virology)</term>
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<term>Survie cellulaire</term>
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<term>Complexe-2 cible mécanistique de la rapamycine</term>
<term>Hépatocytes</term>
<term>Phosphoenolpyruvate carboxykinase (ATP)</term>
<term>Récepteur du peptide-1 similaire au glucagon</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Glucagon-like peptide 1</term>
<term>Liraglutide</term>
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<front><div type="abstract" xml:lang="en">Insulin resistance and diabetes are both associated with chronic hepatitis C virus (HCV) infection, and the glucagon-like peptide-1(GLP-1) receptor agonist, liraglutide, is a common therapy for diabetes. Our aim was to investigate whether liraglutide treatment can inhibit HCV replication. A cell culture-produced HCV infectious system was generated by transfection of in vitro-transcribed genomic JFH-1 ribonucleic acid (RNA) into Huh-7.5 cells. Total RNA samples were extracted to determine the efficiency of HCV replication. The Ava5 cells were treated with liraglutide and cell viability was calculated. A Western blot analysis of the protein expression was performed. The immunoreactive blot signals were also detected. Liraglutide activated GLP-1 receptors in the HCV infectious system, and inhibited subgenomic HCV RNA replication in the HuH-7.5 cells. The Western blot analysis revealed both HCV protein and replicon RNA were reduced after treatment with liraglutide in a dose-dependent manner. Liraglutide decreased the cell viability of HCV RNA at an optimum concentration of 120 μg/mL, activated the 5' adenosine monophosphate-activated protein kinase (AMPK) and the phosphorylated- transducer of regulated cyclic adenosine monophosphate (CAMP) response element-binding protein 2 (TORC2), thereby decreasing the cell viability of phosphoenolpyruvate carboxykinase (PEPCK) and G6pase RNA Therefore, we conclude that liraglutide can inhibit HCV replication via an AMPK/TORC2-dependent pathway.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31540136</PMID>
<DateCompleted><Year>2020</Year>
<Month>02</Month>
<Day>06</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>02</Month>
<Day>06</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1422-0067</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>20</Volume>
<Issue>18</Issue>
<PubDate><Year>2019</Year>
<Month>Sep</Month>
<Day>14</Day>
</PubDate>
</JournalIssue>
<Title>International journal of molecular sciences</Title>
<ISOAbbreviation>Int J Mol Sci</ISOAbbreviation>
</Journal>
<ArticleTitle>Liraglutide Inhibits Hepatitis C Virus Replication Through an AMP Activated Protein Kinase Dependent Mechanism.</ArticleTitle>
<ELocationID EIdType="pii" ValidYN="Y">E4569</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.3390/ijms20184569</ELocationID>
<Abstract><AbstractText>Insulin resistance and diabetes are both associated with chronic hepatitis C virus (HCV) infection, and the glucagon-like peptide-1(GLP-1) receptor agonist, liraglutide, is a common therapy for diabetes. Our aim was to investigate whether liraglutide treatment can inhibit HCV replication. A cell culture-produced HCV infectious system was generated by transfection of in vitro-transcribed genomic JFH-1 ribonucleic acid (RNA) into Huh-7.5 cells. Total RNA samples were extracted to determine the efficiency of HCV replication. The Ava5 cells were treated with liraglutide and cell viability was calculated. A Western blot analysis of the protein expression was performed. The immunoreactive blot signals were also detected. Liraglutide activated GLP-1 receptors in the HCV infectious system, and inhibited subgenomic HCV RNA replication in the HuH-7.5 cells. The Western blot analysis revealed both HCV protein and replicon RNA were reduced after treatment with liraglutide in a dose-dependent manner. Liraglutide decreased the cell viability of HCV RNA at an optimum concentration of 120 μg/mL, activated the 5' adenosine monophosphate-activated protein kinase (AMPK) and the phosphorylated- transducer of regulated cyclic adenosine monophosphate (CAMP) response element-binding protein 2 (TORC2), thereby decreasing the cell viability of phosphoenolpyruvate carboxykinase (PEPCK) and G6pase RNA Therefore, we conclude that liraglutide can inhibit HCV replication via an AMPK/TORC2-dependent pathway.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName>
<ForeName>Mei-Yueh</ForeName>
<Initials>MY</Initials>
<AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan. lovellelee@hotmail.com.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan. lovellelee@hotmail.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Wei-Chun</ForeName>
<Initials>WC</Initials>
<AffiliationInfo><Affiliation>Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan. daphny3016@hotmail.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hsu</LastName>
<ForeName>Wei-Hao</ForeName>
<Initials>WH</Initials>
<AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan. my345677@yahoo.com.tw.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Internal Medicine, Kaohsiung Municipal Siaogang Hospital, Kaohsiung Medical University, Kaohsiung 81267, Taiwan. my345677@yahoo.com.tw.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Szu-Chia</ForeName>
<Initials>SC</Initials>
<Identifier Source="ORCID">0000-0002-1610-4184</Identifier>
<AffiliationInfo><Affiliation>School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan. scarchenone@yahoo.com.tw.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Internal Medicine, Kaohsiung Municipal Siaogang Hospital, Kaohsiung Medical University, Kaohsiung 81267, Taiwan. scarchenone@yahoo.com.tw.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Division of Nephrology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan. scarchenone@yahoo.com.tw.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lee</LastName>
<ForeName>Jin-Ching</ForeName>
<Initials>JC</Initials>
<AffiliationInfo><Affiliation>Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan. jclee@kmu.edu.tw.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Biotechnology, College of Life Science, Kaohsiung Medical University, Kaohsiung 80708, Taiwan. jclee@kmu.edu.tw.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Graduate Institute of Natural Products, College of Pharmacy, Kaohsiung Medical University, Kaohsiung 80708, Taiwan. jclee@kmu.edu.tw.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Drug Development and Value Creation Research Center, Kaohsiung Medical University, Kaohsiung 80708, Taiwan. jclee@kmu.edu.tw.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>MOST104-2320-B-037-025-MY3</GrantID>
<Agency>Ministry of Science and Technology</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>MOST 106-2314-B-037-051</GrantID>
<Agency>Ministry of Science Technology</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>KMU-TP105H02</GrantID>
<Agency>Kaohsiung Medical University under Aim for the Top Universities, Taiwan</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>KMHK-105-016</GrantID>
<Agency>Kaohsiung Municipal Hsiao-Kang Hospital</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>KMTTH-104-032</GrantID>
<Agency>Kaohsiung Municipal Ta-Tung Hospital</Agency>
<Country></Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2019</Year>
<Month>09</Month>
<Day>14</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Switzerland</Country>
<MedlineTA>Int J Mol Sci</MedlineTA>
<NlmUniqueID>101092791</NlmUniqueID>
<ISSNLinking>1422-0067</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000067757">Glucagon-Like Peptide-1 Receptor</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>839I73S42A</RegistryNumber>
<NameOfSubstance UI="D000069450">Liraglutide</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>89750-14-1</RegistryNumber>
<NameOfSubstance UI="D052216">Glucagon-Like Peptide 1</NameOfSubstance>
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<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D000076225">Mechanistic Target of Rapamycin Complex 2</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.31</RegistryNumber>
<NameOfSubstance UI="D055372">AMP-Activated Protein Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 4.1.1.49</RegistryNumber>
<NameOfSubstance UI="C000597251">PCK2 protein, human</NameOfSubstance>
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<Chemical><RegistryNumber>EC 4.1.1.49</RegistryNumber>
<NameOfSubstance UI="D019764">Phosphoenolpyruvate Carboxykinase (ATP)</NameOfSubstance>
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<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D055372" MajorTopicYN="N">AMP-Activated Protein Kinases</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D052216" MajorTopicYN="N">Glucagon-Like Peptide 1</DescriptorName>
<QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
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<MeshHeading><DescriptorName UI="D000067757" MajorTopicYN="N">Glucagon-Like Peptide-1 Receptor</DescriptorName>
<QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016174" MajorTopicYN="N">Hepacivirus</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D022781" MajorTopicYN="N">Hepatocytes</DescriptorName>
<QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000069450" MajorTopicYN="N">Liraglutide</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000076225" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 2</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019764" MajorTopicYN="N">Phosphoenolpyruvate Carboxykinase (ATP)</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">AMPK</Keyword>
<Keyword MajorTopicYN="N">GLP-1</Keyword>
<Keyword MajorTopicYN="N">diabetes mellitus</Keyword>
<Keyword MajorTopicYN="N">hepatitis C virus</Keyword>
<Keyword MajorTopicYN="N">liraglutide</Keyword>
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<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year>
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<Month>08</Month>
<Day>29</Day>
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<PubMedPubDate PubStatus="accepted"><Year>2019</Year>
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<Day>09</Day>
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<affiliations><list><country><li>Taïwan</li>
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<name sortKey="Chen, Wei Chun" sort="Chen, Wei Chun" uniqKey="Chen W" first="Wei-Chun" last="Chen">Wei-Chun Chen</name>
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   |texte=   Liraglutide Inhibits Hepatitis C Virus Replication Through an AMP Activated Protein Kinase Dependent Mechanism.
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Liraglutide Inhibits Hepatitis C Virus Replication Through an AMP Activated Protein Kinase Dependent Mechanism.

Liraglutide Inhibits Hepatitis C Virus Replication Through an AMP Activated Protein Kinase Dependent Mechanism.

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