Insulin inhibits lipolysis in adipocytes via the evolutionarily conserved mTORC1-Egr1-ATGL-mediated pathway.
Identifieur interne : 001028 ( Main/Exploration ); précédent : 001027; suivant : 001029Insulin inhibits lipolysis in adipocytes via the evolutionarily conserved mTORC1-Egr1-ATGL-mediated pathway.
Auteurs : Partha Chakrabarti [États-Unis] ; Ju Youn Kim ; Maneet Singh ; Yu-Kyong Shin ; Jessica Kim ; Joerg Kumbrink ; Yuanyuan Wu ; Mi-Jeong Lee ; Kathrin H. Kirsch ; Susan K. Fried ; Konstantin V. KandrorSource :
- Molecular and cellular biology [ 1098-5549 ] ; 2013.
Descripteurs français
- KwdFr :
- Adipocytes (métabolisme), Animaux (MeSH), Cellules 3T3-L1 (MeSH), Cellules HEK293 (MeSH), Cellules cultivées (MeSH), Complexe-1 cible mécanistique de la rapamycine (MeSH), Complexes multiprotéiques (génétique), Complexes multiprotéiques (métabolisme), Facteur de transcription EGR-1 (génétique), Facteur de transcription EGR-1 (métabolisme), Facteurs de transcription (génétique), Facteurs de transcription (métabolisme), Humains (MeSH), Insuline (métabolisme), Lipolyse (MeSH), Mâle (MeSH), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Protéines de liaison à l'ADN (génétique), Protéines de liaison à l'ADN (métabolisme), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Souris (MeSH), Souris de lignée C57BL (MeSH), Sérine-thréonine kinases TOR (génétique), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (MeSH), Triacylglycerol lipase (génétique), Triacylglycerol lipase (métabolisme), Évolution moléculaire (MeSH).
- MESH :
- génétique : Complexes multiprotéiques, Facteur de transcription EGR-1, Facteurs de transcription, Protéines de Saccharomyces cerevisiae, Protéines de liaison à l'ADN, Saccharomyces cerevisiae, Sérine-thréonine kinases TOR, Triacylglycerol lipase.
- métabolisme : Adipocytes, Complexes multiprotéiques, Facteur de transcription EGR-1, Facteurs de transcription, Insuline, Protéines de Saccharomyces cerevisiae, Protéines de liaison à l'ADN, Saccharomyces cerevisiae, Sérine-thréonine kinases TOR, Triacylglycerol lipase.
- Animaux, Cellules 3T3-L1, Cellules HEK293, Cellules cultivées, Complexe-1 cible mécanistique de la rapamycine, Humains, Lipolyse, Mâle, Souris, Souris de lignée C57BL, Transduction du signal, Évolution moléculaire.
English descriptors
- KwdEn :
- 3T3-L1 Cells (MeSH), Adipocytes (metabolism), Animals (MeSH), Cells, Cultured (MeSH), DNA-Binding Proteins (genetics), DNA-Binding Proteins (metabolism), Early Growth Response Protein 1 (genetics), Early Growth Response Protein 1 (metabolism), Evolution, Molecular (MeSH), HEK293 Cells (MeSH), Humans (MeSH), Insulin (metabolism), Lipase (genetics), Lipase (metabolism), Lipolysis (MeSH), Male (MeSH), Mechanistic Target of Rapamycin Complex 1 (MeSH), Mice (MeSH), Mice, Inbred C57BL (MeSH), Multiprotein Complexes (genetics), Multiprotein Complexes (metabolism), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (metabolism), Transcription Factors (genetics), Transcription Factors (metabolism).
- MESH :
- chemical , genetics : DNA-Binding Proteins, Early Growth Response Protein 1, Lipase, Multiprotein Complexes, Saccharomyces cerevisiae Proteins, TOR Serine-Threonine Kinases, Transcription Factors.
- genetics : Saccharomyces cerevisiae.
- metabolism : Adipocytes, DNA-Binding Proteins, Early Growth Response Protein 1, Insulin, Lipase, Multiprotein Complexes, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, TOR Serine-Threonine Kinases, Transcription Factors.
- 3T3-L1 Cells, Animals, Cells, Cultured, Evolution, Molecular, HEK293 Cells, Humans, Lipolysis, Male, Mechanistic Target of Rapamycin Complex 1, Mice, Mice, Inbred C57BL, Signal Transduction.
Abstract
One of the basic functions of insulin in the body is to inhibit lipolysis in adipocytes. Recently, we have found that insulin inhibits lipolysis and promotes triglyceride storage by decreasing transcription of adipose triglyceride lipase via the mTORC1-mediated pathway (P. Chakrabarti et al., Diabetes 59:775-781, 2010), although the mechanism of this effect remained unknown. Here, we used a genetic screen in Saccharomyces cerevisiae in order to identify a transcription factor that mediates the effect of Tor1 on the expression of the ATGL ortholog in yeast. This factor, Msn4p, has homologues in mammalian cells that form a family of early growth response transcription factors. One member of the family, Egr1, is induced by insulin and nutrients and directly inhibits activity of the ATGL promoter in vitro and expression of ATGL in cultured adipocytes. Feeding animals a high-fat diet increases the activity of mTORC1 and the expression of Egr1 while decreasing ATGL levels in epididymal fat. We suggest that the evolutionarily conserved mTORC1-Egr1-ATGL regulatory pathway represents an important component of the antilipolytic effect of insulin in the mammalian organism.
DOI: 10.1128/MCB.01584-12
PubMed: 23858058
PubMed Central: PMC3753874
Affiliations:
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(MeSH)</term><term>Multiprotein Complexes (genetics)</term><term>Multiprotein Complexes (metabolism)</term><term>Saccharomyces cerevisiae (genetics)</term><term>Saccharomyces cerevisiae (metabolism)</term><term>Saccharomyces cerevisiae Proteins (genetics)</term><term>Saccharomyces cerevisiae Proteins (metabolism)</term><term>Signal Transduction (MeSH)</term><term>TOR Serine-Threonine Kinases (genetics)</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Transcription Factors (genetics)</term><term>Transcription Factors (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adipocytes (métabolisme)</term><term>Animaux (MeSH)</term><term>Cellules 3T3-L1 (MeSH)</term><term>Cellules HEK293 (MeSH)</term><term>Cellules cultivées (MeSH)</term><term>Complexe-1 cible mécanistique de la rapamycine (MeSH)</term><term>Complexes multiprotéiques (génétique)</term><term>Complexes multiprotéiques (métabolisme)</term><term>Facteur de transcription EGR-1 (génétique)</term><term>Facteur de transcription EGR-1 (métabolisme)</term><term>Facteurs de transcription (génétique)</term><term>Facteurs de transcription (métabolisme)</term><term>Humains (MeSH)</term><term>Insuline (métabolisme)</term><term>Lipolyse (MeSH)</term><term>Mâle (MeSH)</term><term>Protéines de Saccharomyces cerevisiae (génétique)</term><term>Protéines de Saccharomyces cerevisiae (métabolisme)</term><term>Protéines de liaison à l'ADN (génétique)</term><term>Protéines de liaison à l'ADN (métabolisme)</term><term>Saccharomyces cerevisiae (génétique)</term><term>Saccharomyces cerevisiae (métabolisme)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term><term>Sérine-thréonine kinases TOR (génétique)</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Transduction du signal (MeSH)</term><term>Triacylglycerol lipase (génétique)</term><term>Triacylglycerol lipase (métabolisme)</term><term>Évolution moléculaire (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA-Binding Proteins</term><term>Early Growth Response Protein 1</term><term>Lipase</term><term>Multiprotein Complexes</term><term>Saccharomyces cerevisiae Proteins</term><term>TOR Serine-Threonine Kinases</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Complexes multiprotéiques</term><term>Facteur de transcription EGR-1</term><term>Facteurs de transcription</term><term>Protéines de Saccharomyces cerevisiae</term><term>Protéines de liaison à l'ADN</term><term>Saccharomyces cerevisiae</term><term>Sérine-thréonine kinases TOR</term><term>Triacylglycerol lipase</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Adipocytes</term><term>DNA-Binding Proteins</term><term>Early Growth Response Protein 1</term><term>Insulin</term><term>Lipase</term><term>Multiprotein Complexes</term><term>Saccharomyces cerevisiae</term><term>Saccharomyces cerevisiae Proteins</term><term>TOR Serine-Threonine Kinases</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Adipocytes</term><term>Complexes multiprotéiques</term><term>Facteur de transcription EGR-1</term><term>Facteurs de transcription</term><term>Insuline</term><term>Protéines de Saccharomyces cerevisiae</term><term>Protéines de liaison à l'ADN</term><term>Saccharomyces cerevisiae</term><term>Sérine-thréonine kinases TOR</term><term>Triacylglycerol lipase</term></keywords><keywords scheme="MESH" xml:lang="en"><term>3T3-L1 Cells</term><term>Animals</term><term>Cells, Cultured</term><term>Evolution, Molecular</term><term>HEK293 Cells</term><term>Humans</term><term>Lipolysis</term><term>Male</term><term>Mechanistic Target of Rapamycin Complex 1</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules 3T3-L1</term><term>Cellules HEK293</term><term>Cellules cultivées</term><term>Complexe-1 cible mécanistique de la rapamycine</term><term>Humains</term><term>Lipolyse</term><term>Mâle</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Transduction du signal</term><term>Évolution moléculaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">One of the basic functions of insulin in the body is to inhibit lipolysis in adipocytes. Recently, we have found that insulin inhibits lipolysis and promotes triglyceride storage by decreasing transcription of adipose triglyceride lipase via the mTORC1-mediated pathway (P. Chakrabarti et al., Diabetes 59:775-781, 2010), although the mechanism of this effect remained unknown. Here, we used a genetic screen in Saccharomyces cerevisiae in order to identify a transcription factor that mediates the effect of Tor1 on the expression of the ATGL ortholog in yeast. This factor, Msn4p, has homologues in mammalian cells that form a family of early growth response transcription factors. One member of the family, Egr1, is induced by insulin and nutrients and directly inhibits activity of the ATGL promoter in vitro and expression of ATGL in cultured adipocytes. Feeding animals a high-fat diet increases the activity of mTORC1 and the expression of Egr1 while decreasing ATGL levels in epididymal fat. We suggest that the evolutionarily conserved mTORC1-Egr1-ATGL regulatory pathway represents an important component of the antilipolytic effect of insulin in the mammalian organism. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23858058</PMID><DateCompleted><Year>2013</Year><Month>11</Month><Day>25</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5549</ISSN><JournalIssue CitedMedium="Internet"><Volume>33</Volume><Issue>18</Issue><PubDate><Year>2013</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Molecular and cellular biology</Title><ISOAbbreviation>Mol Cell Biol</ISOAbbreviation></Journal><ArticleTitle>Insulin inhibits lipolysis in adipocytes via the evolutionarily conserved mTORC1-Egr1-ATGL-mediated pathway.</ArticleTitle><Pagination><MedlinePgn>3659-66</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/MCB.01584-12</ELocationID><Abstract><AbstractText>One of the basic functions of insulin in the body is to inhibit lipolysis in adipocytes. Recently, we have found that insulin inhibits lipolysis and promotes triglyceride storage by decreasing transcription of adipose triglyceride lipase via the mTORC1-mediated pathway (P. Chakrabarti et al., Diabetes 59:775-781, 2010), although the mechanism of this effect remained unknown. Here, we used a genetic screen in Saccharomyces cerevisiae in order to identify a transcription factor that mediates the effect of Tor1 on the expression of the ATGL ortholog in yeast. This factor, Msn4p, has homologues in mammalian cells that form a family of early growth response transcription factors. One member of the family, Egr1, is induced by insulin and nutrients and directly inhibits activity of the ATGL promoter in vitro and expression of ATGL in cultured adipocytes. Feeding animals a high-fat diet increases the activity of mTORC1 and the expression of Egr1 while decreasing ATGL levels in epididymal fat. We suggest that the evolutionarily conserved mTORC1-Egr1-ATGL regulatory pathway represents an important component of the antilipolytic effect of insulin in the mammalian organism. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chakrabarti</LastName><ForeName>Partha</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Boston University School of Medicine, Boston, Massachusetts, USA. pc1@csiriicb.in</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Ju Youn</ForeName><Initials>JY</Initials></Author><Author ValidYN="Y"><LastName>Singh</LastName><ForeName>Maneet</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Shin</LastName><ForeName>Yu-Kyong</ForeName><Initials>YK</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Jessica</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Kumbrink</LastName><ForeName>Joerg</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Yuanyuan</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Mi-Jeong</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Kirsch</LastName><ForeName>Kathrin H</ForeName><Initials>KH</Initials></Author><Author ValidYN="Y"><LastName>Fried</LastName><ForeName>Susan K</ForeName><Initials>SK</Initials></Author><Author ValidYN="Y"><LastName>Kandror</LastName><ForeName>Konstantin V</ForeName><Initials>KV</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R21 AG039612</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AG039612</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R56 DK052057</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DK052057</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>DK52057</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>07</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mol Cell Biol</MedlineTA><NlmUniqueID>8109087</NlmUniqueID><ISSNLinking>0270-7306</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004268">DNA-Binding Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051766">Early Growth Response Protein 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C486109">Egr1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C081937">MSN4 protein, S cerevisiae</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D046912">Multiprotein Complexes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029701">Saccharomyces cerevisiae Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D000076222">Mechanistic Target of Rapamycin Complex 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.1.3</RegistryNumber><NameOfSubstance UI="D008049">Lipase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.1.3</RegistryNumber><NameOfSubstance UI="C494445">PNPLA2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.1.3</RegistryNumber><NameOfSubstance UI="C506904">Tgl4 protein, S cerevisiae</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D041721" MajorTopicYN="N">3T3-L1 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Fried</name><name sortKey="Kandror, Konstantin V" sort="Kandror, Konstantin V" uniqKey="Kandror K" first="Konstantin V" last="Kandror">Konstantin V. Kandror</name><name sortKey="Kim, Jessica" sort="Kim, Jessica" uniqKey="Kim J" first="Jessica" last="Kim">Jessica Kim</name><name sortKey="Kim, Ju Youn" sort="Kim, Ju Youn" uniqKey="Kim J" first="Ju Youn" last="Kim">Ju Youn Kim</name><name sortKey="Kirsch, Kathrin H" sort="Kirsch, Kathrin H" uniqKey="Kirsch K" first="Kathrin H" last="Kirsch">Kathrin H. Kirsch</name><name sortKey="Kumbrink, Joerg" sort="Kumbrink, Joerg" uniqKey="Kumbrink J" first="Joerg" last="Kumbrink">Joerg Kumbrink</name><name sortKey="Lee, Mi Jeong" sort="Lee, Mi Jeong" uniqKey="Lee M" first="Mi-Jeong" last="Lee">Mi-Jeong Lee</name><name sortKey="Shin, Yu Kyong" sort="Shin, Yu Kyong" uniqKey="Shin Y" first="Yu-Kyong" last="Shin">Yu-Kyong Shin</name><name sortKey="Singh, Maneet" sort="Singh, Maneet" uniqKey="Singh M" first="Maneet" last="Singh">Maneet Singh</name><name sortKey="Wu, Yuanyuan" sort="Wu, Yuanyuan" uniqKey="Wu Y" first="Yuanyuan" last="Wu">Yuanyuan Wu</name></noCountry><country name="États-Unis"><region name="Massachusetts"><name sortKey="Chakrabarti, Partha" sort="Chakrabarti, Partha" uniqKey="Chakrabarti P" first="Partha" last="Chakrabarti">Partha Chakrabarti</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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