Sodium tungstate activates glycogen synthesis through a non-canonical mechanism involving G-proteins.
Identifieur interne : 000147 ( Main/Exploration ); précédent : 000146; suivant : 000148Sodium tungstate activates glycogen synthesis through a non-canonical mechanism involving G-proteins.
Auteurs : Delia Zafra [Espagne] ; Laura Nocito ; Jorge Domínguez ; Joan J. GuinovartSource :
- FEBS letters [ 1873-3468 ] ; 2013.
Descripteurs français
- KwdFr :
- Activation enzymatique (effets des médicaments et des substances chimiques), Animaux (MeSH), Cellules CHO (MeSH), Composés du tungstène (pharmacologie), Cricetinae (MeSH), Cricetulus (MeSH), Extracellular Signal-Regulated MAP Kinases (métabolisme), Glycogène (biosynthèse), Humains (MeSH), Hypoglycémiants (pharmacologie), Hépatocytes (cytologie), Hépatocytes (effets des médicaments et des substances chimiques), Hépatocytes (métabolisme), Phosphorylation (effets des médicaments et des substances chimiques), Protéines G hétérotrimériques (métabolisme), Protéines G ras (métabolisme), Rat Wistar (MeSH), Rats (MeSH), Récepteur à l'insuline (génétique), Transduction du signal (effets des médicaments et des substances chimiques), Transfection (MeSH).
- MESH :
- biosynthèse : Glycogène.
- cytologie : Hépatocytes.
- effets des médicaments et des substances chimiques : Activation enzymatique, Hépatocytes, Phosphorylation, Transduction du signal.
- génétique : Récepteur à l'insuline.
- métabolisme : Extracellular Signal-Regulated MAP Kinases, Hépatocytes, Protéines G hétérotrimériques, Protéines G ras.
- pharmacologie : Composés du tungstène, Hypoglycémiants.
- Animaux, Cellules CHO, Cricetinae, Cricetulus, Humains, Rat Wistar, Rats, Transfection.
English descriptors
- KwdEn :
- Animals (MeSH), CHO Cells (MeSH), Cricetinae (MeSH), Cricetulus (MeSH), Enzyme Activation (drug effects), Extracellular Signal-Regulated MAP Kinases (metabolism), Glycogen (biosynthesis), Hepatocytes (cytology), Hepatocytes (drug effects), Hepatocytes (metabolism), Heterotrimeric GTP-Binding Proteins (metabolism), Humans (MeSH), Hypoglycemic Agents (pharmacology), Phosphorylation (drug effects), Rats (MeSH), Rats, Wistar (MeSH), Receptor, Insulin (genetics), Signal Transduction (drug effects), Transfection (MeSH), Tungsten Compounds (pharmacology), ras Proteins (metabolism).
- MESH :
- chemical , biosynthesis : Glycogen.
- chemical , genetics : Receptor, Insulin.
- chemical , metabolism : Extracellular Signal-Regulated MAP Kinases, Heterotrimeric GTP-Binding Proteins, ras Proteins.
- cytology : Hepatocytes.
- drug effects : Enzyme Activation, Hepatocytes, Phosphorylation, Signal Transduction.
- metabolism : Hepatocytes.
- chemical , pharmacology : Hypoglycemic Agents, Tungsten Compounds.
- Animals, CHO Cells, Cricetinae, Cricetulus, Humans, Rats, Rats, Wistar, Transfection.
Abstract
Tungstate treatment ameliorates experimental diabetes by increasing liver glycogen deposition through an as yet unidentified mechanism. The signalling mechanism of tungstate was studied in CHOIR cells and primary cultured hepatocytes. This compound exerted its pro-glycogenic effects through a new G-protein-dependent and Tyr-Kinase Receptor-independent mechanism. Chemical or genetic disruption of G-protein signalling prevented the activation of the Ras/ERK cascade and the downstream induction of glycogen synthesis caused by tungstate. Thus, these findings unveil a novel non-canonical signalling pathway that leads to the activation of glycogen synthesis and that could be exploited as an approach to treat diabetes.
DOI: 10.1016/j.febslet.2012.11.034
PubMed: 23260418
Affiliations:
Links toward previous steps (curation, corpus...)
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The signalling mechanism of tungstate was studied in CHOIR cells and primary cultured hepatocytes. This compound exerted its pro-glycogenic effects through a new G-protein-dependent and Tyr-Kinase Receptor-independent mechanism. Chemical or genetic disruption of G-protein signalling prevented the activation of the Ras/ERK cascade and the downstream induction of glycogen synthesis caused by tungstate. Thus, these findings unveil a novel non-canonical signalling pathway that leads to the activation of glycogen synthesis and that could be exploited as an approach to treat diabetes.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23260418</PMID><DateCompleted><Year>2013</Year><Month>03</Month><Day>21</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-3468</ISSN><JournalIssue CitedMedium="Internet"><Volume>587</Volume><Issue>3</Issue><PubDate><Year>2013</Year><Month>Jan</Month><Day>31</Day></PubDate></JournalIssue><Title>FEBS letters</Title></Journal><ArticleTitle>Sodium tungstate activates glycogen synthesis through a non-canonical mechanism involving G-proteins.</ArticleTitle><Pagination><MedlinePgn>291-6</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.febslet.2012.11.034</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0014-5793(12)00911-8</ELocationID><Abstract><AbstractText>Tungstate treatment ameliorates experimental diabetes by increasing liver glycogen deposition through an as yet unidentified mechanism. The signalling mechanism of tungstate was studied in CHOIR cells and primary cultured hepatocytes. This compound exerted its pro-glycogenic effects through a new G-protein-dependent and Tyr-Kinase Receptor-independent mechanism. Chemical or genetic disruption of G-protein signalling prevented the activation of the Ras/ERK cascade and the downstream induction of glycogen synthesis caused by tungstate. Thus, these findings unveil a novel non-canonical signalling pathway that leads to the activation of glycogen synthesis and that could be exploited as an approach to treat diabetes.</AbstractText><CopyrightInformation>Copyright © 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zafra</LastName><ForeName>Delia</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Institute for Research in Biomedicine (IRB Barcelona) and Department of Biochemistry and Molecular Biology, University of Barcelona, and CIBER de Diabetes y Enfermedades Metabólicas (CIBERDEM), Baldiri Reixac 10-12, E-08028 Barcelona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nocito</LastName><ForeName>Laura</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Domínguez</LastName><ForeName>Jorge</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Guinovart</LastName><ForeName>Joan J</ForeName><Initials>JJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>12</Month><Day>19</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>FEBS Lett</MedlineTA><NlmUniqueID>0155157</NlmUniqueID><ISSNLinking>0014-5793</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017973">Tungsten Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>64LRH4405G</RegistryNumber><NameOfSubstance UI="C025399">sodium tungstate(VI)</NameOfSubstance></Chemical><Chemical><RegistryNumber>9005-79-2</RegistryNumber><NameOfSubstance UI="D006003">Glycogen</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D011972">Receptor, Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 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UI="D014162" MajorTopicYN="N">Transfection</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017973" MajorTopicYN="N">Tungsten Compounds</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018631" MajorTopicYN="N">ras Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>08</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2012</Year><Month>11</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2012</Year><Month>11</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>12</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>12</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>3</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23260418</ArticleId><ArticleId IdType="pii">S0014-5793(12)00911-8</ArticleId><ArticleId IdType="doi">10.1016/j.febslet.2012.11.034</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Espagne</li></country><region><li>Catalogne</li></region></list><tree><noCountry><name sortKey="Dominguez, Jorge" sort="Dominguez, Jorge" uniqKey="Dominguez J" first="Jorge" last="Domínguez">Jorge Domínguez</name><name sortKey="Guinovart, Joan J" sort="Guinovart, Joan J" uniqKey="Guinovart J" first="Joan J" last="Guinovart">Joan J. Guinovart</name><name sortKey="Nocito, Laura" sort="Nocito, Laura" uniqKey="Nocito L" first="Laura" last="Nocito">Laura Nocito</name></noCountry><country name="Espagne"><region name="Catalogne"><name sortKey="Zafra, Delia" sort="Zafra, Delia" uniqKey="Zafra D" first="Delia" last="Zafra">Delia Zafra</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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