Glucagon and Insulin Cooperatively Stimulate Fibroblast Growth Factor 21 Gene Transcription by Increasing the Expression of Activating Transcription Factor 4.
Identifieur interne : 000835 ( Main/Exploration ); précédent : 000834; suivant : 000836Glucagon and Insulin Cooperatively Stimulate Fibroblast Growth Factor 21 Gene Transcription by Increasing the Expression of Activating Transcription Factor 4.
Auteurs : Kimberly M. Alonge ; Gordon P. Meares [États-Unis] ; F Bradley Hillgartner [États-Unis]Source :
- The Journal of biological chemistry [ 1083-351X ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Cellules cultivées (MeSH), Chénodiol (pharmacologie), Facteur de transcription ATF-4 (métabolisme), Facteur-2 d'initiation eucaryote (pharmacologie), Facteurs de croissance fibroblastique (génétique), Glucagon (pharmacologie), Glucagon (physiologie), Hépatocytes (cytologie), Insuline (physiologie), Rats (MeSH), Régulation de l'expression des gènes (effets des médicaments et des substances chimiques), Synergie des médicaments (MeSH), Transcription génétique (effets des médicaments et des substances chimiques).
- MESH :
- cytologie : Hépatocytes.
- effets des médicaments et des substances chimiques : Régulation de l'expression des gènes, Transcription génétique.
- génétique : Facteurs de croissance fibroblastique.
- métabolisme : Facteur de transcription ATF-4.
- pharmacologie : Chénodiol, Facteur-2 d'initiation eucaryote, Glucagon.
- physiologie : Glucagon, Insuline.
- Animaux, Cellules cultivées, Rats, Synergie des médicaments.
English descriptors
- KwdEn :
- Activating Transcription Factor 4 (metabolism), Animals (MeSH), Cells, Cultured (MeSH), Chenodeoxycholic Acid (pharmacology), Drug Synergism (MeSH), Eukaryotic Initiation Factor-2 (pharmacology), Fibroblast Growth Factors (genetics), Gene Expression Regulation (drug effects), Glucagon (pharmacology), Glucagon (physiology), Hepatocytes (cytology), Insulin (physiology), Rats (MeSH), Transcription, Genetic (drug effects).
- MESH :
- chemical , genetics : Fibroblast Growth Factors.
- chemical , metabolism : Activating Transcription Factor 4.
- chemical , pharmacology : Chenodeoxycholic Acid, Eukaryotic Initiation Factor-2, Glucagon.
- cytology : Hepatocytes.
- drug effects : Gene Expression Regulation, Transcription, Genetic.
- chemical , physiology : Glucagon, Insulin.
- Animals, Cells, Cultured, Drug Synergism, Rats.
Abstract
Previous studies have shown that glucagon cooperatively interacts with insulin to stimulate hepatic FGF21 gene expression. Here we investigated the mechanism by which glucagon and insulin increased FGF21 gene transcription in primary hepatocyte cultures. Transfection analyses demonstrated that glucagon plus insulin induction of FGF21 transcription was conferred by two activating transcription factor 4 (ATF4) binding sites in the FGF21 gene. Glucagon plus insulin stimulated a 5-fold increase in ATF4 protein abundance, and knockdown of ATF4 expression suppressed the ability of glucagon plus insulin to increase FGF21 expression. In hepatocytes incubated in the presence of insulin, treatment with a PKA-selective agonist mimicked the ability of glucagon to stimulate ATF4 and FGF21 expression. Inhibition of PKA, PI3K, Akt, and mammalian target of rapamycin complex 1 (mTORC1) suppressed the ability of glucagon plus insulin to stimulate ATF4 and FGF21 expression. Additional analyses demonstrated that chenodeoxycholic acid (CDCA) induced a 6-fold increase in ATF4 expression and that knockdown of ATF4 expression suppressed the ability of CDCA to increase FGF21 gene expression. CDCA increased the phosphorylation of eIF2α, and inhibition of eIF2α signaling activity suppressed CDCA regulation of ATF4 and FGF21 expression. These results demonstrate that glucagon plus insulin increases FGF21 transcription by stimulating ATF4 expression and that activation of cAMP/PKA and PI3K/Akt/mTORC1 mediates the effect of glucagon plus insulin on ATF4 expression. These results also demonstrate that CDCA regulation of FGF21 transcription is mediated at least partially by an eIF2α-dependent increase in ATF4 expression.
DOI: 10.1074/jbc.M116.762922
PubMed: 28188284
PubMed Central: PMC5392671
Affiliations:
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Le document en format XML
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Meares</name><affiliation wicri:level="2"><nlm:affiliation>Microbiology, Immunology, and Cell Biology, West Virginia University, Morgantown, West Virginia 26506.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Virginie-Occidentale</region></placeName><wicri:cityArea>Microbiology, Immunology, and Cell Biology, West Virginia University, Morgantown</wicri:cityArea></affiliation></author><author><name sortKey="Hillgartner, F Bradley" sort="Hillgartner, F Bradley" uniqKey="Hillgartner F" first="F Bradley" last="Hillgartner">F Bradley Hillgartner</name><affiliation wicri:level="1"><nlm:affiliation>From the Departments of Biochemistry and fbhillgartner@hsc.wvu.edu.</nlm:affiliation><country wicri:rule="url">États-Unis</country></affiliation></author></analytic><series><title level="j">The Journal of biological chemistry</title><idno type="eISSN">1083-351X</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Activating Transcription Factor 4 (metabolism)</term><term>Animals (MeSH)</term><term>Cells, Cultured (MeSH)</term><term>Chenodeoxycholic Acid (pharmacology)</term><term>Drug Synergism (MeSH)</term><term>Eukaryotic Initiation Factor-2 (pharmacology)</term><term>Fibroblast Growth Factors (genetics)</term><term>Gene Expression Regulation (drug effects)</term><term>Glucagon (pharmacology)</term><term>Glucagon (physiology)</term><term>Hepatocytes (cytology)</term><term>Insulin (physiology)</term><term>Rats (MeSH)</term><term>Transcription, Genetic (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Cellules cultivées (MeSH)</term><term>Chénodiol (pharmacologie)</term><term>Facteur de transcription ATF-4 (métabolisme)</term><term>Facteur-2 d'initiation eucaryote (pharmacologie)</term><term>Facteurs de croissance fibroblastique (génétique)</term><term>Glucagon (pharmacologie)</term><term>Glucagon (physiologie)</term><term>Hépatocytes (cytologie)</term><term>Insuline (physiologie)</term><term>Rats (MeSH)</term><term>Régulation de l'expression des gènes (effets des médicaments et des substances chimiques)</term><term>Synergie des médicaments (MeSH)</term><term>Transcription génétique (effets des médicaments et des substances chimiques)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Fibroblast Growth Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Activating Transcription Factor 4</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Chenodeoxycholic Acid</term><term>Eukaryotic Initiation Factor-2</term><term>Glucagon</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Hépatocytes</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Hepatocytes</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression Regulation</term><term>Transcription, Genetic</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Régulation de l'expression des gènes</term><term>Transcription génétique</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteurs de croissance fibroblastique</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur de transcription ATF-4</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Chénodiol</term><term>Facteur-2 d'initiation eucaryote</term><term>Glucagon</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Glucagon</term><term>Insuline</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Glucagon</term><term>Insulin</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Drug Synergism</term><term>Rats</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Rats</term><term>Synergie des médicaments</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Previous studies have shown that glucagon cooperatively interacts with insulin to stimulate hepatic FGF21 gene expression. Here we investigated the mechanism by which glucagon and insulin increased FGF21 gene transcription in primary hepatocyte cultures. Transfection analyses demonstrated that glucagon plus insulin induction of FGF21 transcription was conferred by two activating transcription factor 4 (ATF4) binding sites in the FGF21 gene. Glucagon plus insulin stimulated a 5-fold increase in ATF4 protein abundance, and knockdown of ATF4 expression suppressed the ability of glucagon plus insulin to increase FGF21 expression. In hepatocytes incubated in the presence of insulin, treatment with a PKA-selective agonist mimicked the ability of glucagon to stimulate ATF4 and FGF21 expression. Inhibition of PKA, PI3K, Akt, and mammalian target of rapamycin complex 1 (mTORC1) suppressed the ability of glucagon plus insulin to stimulate ATF4 and FGF21 expression. Additional analyses demonstrated that chenodeoxycholic acid (CDCA) induced a 6-fold increase in ATF4 expression and that knockdown of ATF4 expression suppressed the ability of CDCA to increase FGF21 gene expression. CDCA increased the phosphorylation of eIF2α, and inhibition of eIF2α signaling activity suppressed CDCA regulation of ATF4 and FGF21 expression. These results demonstrate that glucagon plus insulin increases FGF21 transcription by stimulating ATF4 expression and that activation of cAMP/PKA and PI3K/Akt/mTORC1 mediates the effect of glucagon plus insulin on ATF4 expression. These results also demonstrate that CDCA regulation of FGF21 transcription is mediated at least partially by an eIF2α-dependent increase in ATF4 expression.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28188284</PMID><DateCompleted><Year>2017</Year><Month>06</Month><Day>12</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1083-351X</ISSN><JournalIssue CitedMedium="Internet"><Volume>292</Volume><Issue>13</Issue><PubDate><Year>2017</Year><Month>03</Month><Day>31</Day></PubDate></JournalIssue><Title>The Journal of biological chemistry</Title><ISOAbbreviation>J Biol Chem</ISOAbbreviation></Journal><ArticleTitle>Glucagon and Insulin Cooperatively Stimulate Fibroblast Growth Factor 21 Gene Transcription by Increasing the Expression of Activating Transcription Factor 4.</ArticleTitle><Pagination><MedlinePgn>5239-5252</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1074/jbc.M116.762922</ELocationID><Abstract><AbstractText>Previous studies have shown that glucagon cooperatively interacts with insulin to stimulate hepatic FGF21 gene expression. Here we investigated the mechanism by which glucagon and insulin increased FGF21 gene transcription in primary hepatocyte cultures. Transfection analyses demonstrated that glucagon plus insulin induction of FGF21 transcription was conferred by two activating transcription factor 4 (ATF4) binding sites in the FGF21 gene. Glucagon plus insulin stimulated a 5-fold increase in ATF4 protein abundance, and knockdown of ATF4 expression suppressed the ability of glucagon plus insulin to increase FGF21 expression. In hepatocytes incubated in the presence of insulin, treatment with a PKA-selective agonist mimicked the ability of glucagon to stimulate ATF4 and FGF21 expression. Inhibition of PKA, PI3K, Akt, and mammalian target of rapamycin complex 1 (mTORC1) suppressed the ability of glucagon plus insulin to stimulate ATF4 and FGF21 expression. Additional analyses demonstrated that chenodeoxycholic acid (CDCA) induced a 6-fold increase in ATF4 expression and that knockdown of ATF4 expression suppressed the ability of CDCA to increase FGF21 gene expression. CDCA increased the phosphorylation of eIF2α, and inhibition of eIF2α signaling activity suppressed CDCA regulation of ATF4 and FGF21 expression. These results demonstrate that glucagon plus insulin increases FGF21 transcription by stimulating ATF4 expression and that activation of cAMP/PKA and PI3K/Akt/mTORC1 mediates the effect of glucagon plus insulin on ATF4 expression. These results also demonstrate that CDCA regulation of FGF21 transcription is mediated at least partially by an eIF2α-dependent increase in ATF4 expression.</AbstractText><CopyrightInformation>© 2017 by The American Society for Biochemistry and Molecular Biology, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Alonge</LastName><ForeName>Kimberly M</ForeName><Initials>KM</Initials><AffiliationInfo><Affiliation>From the Departments of Biochemistry and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meares</LastName><ForeName>Gordon P</ForeName><Initials>GP</Initials><AffiliationInfo><Affiliation>Microbiology, Immunology, and Cell Biology, West Virginia University, Morgantown, West Virginia 26506.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hillgartner</LastName><ForeName>F Bradley</ForeName><Initials>FB</Initials><AffiliationInfo><Affiliation>From the Departments of Biochemistry and fbhillgartner@hsc.wvu.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>T32 HL007028</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U54 GM104942</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>02</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Biol Chem</MedlineTA><NlmUniqueID>2985121R</NlmUniqueID><ISSNLinking>0021-9258</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015852">Eukaryotic Initiation Factor-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C414620">fibroblast growth factor 21</NameOfSubstance></Chemical><Chemical><RegistryNumber>0GEI24LG0J</RegistryNumber><NameOfSubstance UI="D002635">Chenodeoxycholic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>145891-90-3</RegistryNumber><NameOfSubstance UI="D051701">Activating Transcription Factor 4</NameOfSubstance></Chemical><Chemical><RegistryNumber>62031-54-3</RegistryNumber><NameOfSubstance UI="D005346">Fibroblast Growth Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>9007-92-5</RegistryNumber><NameOfSubstance UI="D005934">Glucagon</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D051701" MajorTopicYN="N">Activating Transcription Factor 4</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002635" MajorTopicYN="N">Chenodeoxycholic Acid</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004357" MajorTopicYN="N">Drug Synergism</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015852" MajorTopicYN="N">Eukaryotic Initiation Factor-2</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005346" MajorTopicYN="N">Fibroblast Growth Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005934" MajorTopicYN="N">Glucagon</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D022781" MajorTopicYN="N">Hepatocytes</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014158" MajorTopicYN="N">Transcription, Genetic</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">PKA</Keyword><Keyword MajorTopicYN="Y">bile acid</Keyword><Keyword MajorTopicYN="Y">eIF2</Keyword><Keyword MajorTopicYN="Y">glucagon</Keyword><Keyword MajorTopicYN="Y">insulin</Keyword><Keyword MajorTopicYN="Y">liver</Keyword><Keyword MajorTopicYN="Y">mammalian target of rapamycin (mTOR)</Keyword><Keyword MajorTopicYN="Y">transcription regulation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>10</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>02</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>2</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>6</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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Alonge</name></noCountry><country name="États-Unis"><region name="Virginie-Occidentale"><name sortKey="Meares, Gordon P" sort="Meares, Gordon P" uniqKey="Meares G" first="Gordon P" last="Meares">Gordon P. Meares</name></region><name sortKey="Hillgartner, F Bradley" sort="Hillgartner, F Bradley" uniqKey="Hillgartner F" first="F Bradley" last="Hillgartner">F Bradley Hillgartner</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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