Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/48250
DC FieldValueLanguage
dc.contributor.authorZadjali, Fahaden_US
dc.contributor.authorSantana-Farre, Ruymanen_US
dc.contributor.authorVesterlund, Mattiasen_US
dc.contributor.authorCarow, Beriten_US
dc.contributor.authorMirecki-Garrido, Mercedesen_US
dc.contributor.authorHernandez-Hernandez, Ireneen_US
dc.contributor.authorFlodström-Tullberg, Malinen_US
dc.contributor.authorParini, Paoloen_US
dc.contributor.authorRottenberg, Martinen_US
dc.contributor.authorNorstedt, Gunnaren_US
dc.contributor.authorFernandez-Perez, Leandroen_US
dc.contributor.authorFlores-Morales, Amilcaren_US
dc.contributor.otherHernandez, Irene-
dc.contributor.otherFernandez-Perez, Leandro-
dc.contributor.otherMirecki-Garrido, Mercedes-
dc.contributor.otherZADJALI, FAHAD-
dc.contributor.otherFlodstrom Tullberg, Malin-
dc.contributor.otherVesterlund, Mattias-
dc.contributor.otherNorstedt, Gunnar-
dc.contributor.otherCarow, Berit-
dc.date.accessioned2018-11-23T20:09:06Z-
dc.date.available2018-11-23T20:09:06Z-
dc.date.issued2012en_US
dc.identifier.issn0892-6638en_US
dc.identifier.urihttp://hdl.handle.net/10553/48250-
dc.description.abstractHepatic steatosis is a prominent feature in patients with growth hormone (GH) deficiency. The ubiquitin ligase SOCS2 attenuates hepatic GH signaling by inhibiting the Janus kinase 2 (JAK2)-signal transducer and activator of transcription 5b (STAT5b) axis. Here, we investigated the role of SOCS2 in the development of diet-induced hepatic steatosis and insulin resistance. SOCS2-knockout (SOCS2(-/-)) mice and wild-type littermates were fed for 4 mo with control or high-fat diet, followed by assessment of insulin sensitivity, hepatic lipid content, and expression of inflammatory cytokines. SOCS2(-/-) mice exhibited increased hepatic TG secretion by 77.6% (P<0.001) as compared with wild-type control mice and were protected from high-fat-diet (HFD)-induced hepatic steatosis, showing 49.3% (P<0.01) reduction in liver TG levels compared to HFD-fed wild-type littermates. In contrast, we found that HFD-triggered attenuation of systemic insulin sensitivity was more marked in SOCS2(-/-) mice. Livers from the HFD-fed SOCS2(-/-) mice showed increased NF-kappa B activity as well as elevated expression of genes for the inflammatory cytokines IFN-gamma and IL-6. An inhibitory role of SOCS2 on Toll-like receptor 4 signaling was demonstrated in macrophages obtained from the SOCS2(-/-) and wild-type mice. This study identified SOCS2 as an important regulator of hepatic homeostasis under conditions of high-fat dietary stress.-Zadjali, F., Santana-Farre, R., Vesterlund, M., Carow, B., Mirecki-Garrido, M., Hernandez-Hernandez, I., Flodstrom-Tullberg, M., Parini, P., Rottenberg, M., Norstedt, G., Fernandez-Perez, L., Flores-Morales, A. SOCS2 deletion protects against hepatic steatosis but worsens insulin resistance in high-fat-diet-fed mice.en_US
dc.languageengen_US
dc.relationEstudio Funcional y Molecular de Las Proteínas Socs en Un Modelo de Resistencia Hepática A Insulina.en_US
dc.relation.ispartofFASEB Journalen_US
dc.sourceFaseb Journal[ISSN 0892-6638],v. 26 (8), p. 3282-3291en_US
dc.subject32 Ciencias médicasen_US
dc.subject2302 Bioquímicaen_US
dc.subject.otherLacking Suppressoren_US
dc.subject.otherLiveren_US
dc.subject.otherDeficiencyen_US
dc.subject.otherObesityen_US
dc.subject.otherSteatohepatitisen_US
dc.subject.otherHyperlipidemiaen_US
dc.subject.otherExpressionen_US
dc.subject.otherProteinsen_US
dc.titleSOCS2 deletion protects against hepatic steatosis but worsens insulin resistance in high-fat-diet-fed miceen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1096/fj.12-205583en_US
dc.identifier.scopus84864665833-
dc.identifier.isi000307162800019-
dcterms.isPartOfFaseb Journal-
dcterms.sourceFaseb Journal[ISSN 0892-6638],v. 26 (8), p. 3282-3291-
dc.contributor.authorscopusid23011004900-
dc.contributor.authorscopusid15830358800-
dc.contributor.authorscopusid37091811900-
dc.contributor.authorscopusid35572948200-
dc.contributor.authorscopusid55221793700-
dc.contributor.authorscopusid57201434068-
dc.contributor.authorscopusid8570437300-
dc.contributor.authorscopusid6701425383-
dc.contributor.authorscopusid7003474126-
dc.contributor.authorscopusid7006397634-
dc.contributor.authorscopusid6506777525-
dc.contributor.authorscopusid57203543352-
dc.contributor.authorscopusid57203543358-
dc.description.lastpage3291en_US
dc.description.firstpage3282en_US
dc.relation.volume26en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.identifier.wosWOS:000307162800019-
dc.contributor.daisngid1793904-
dc.contributor.daisngid3808417-
dc.contributor.daisngid2087322-
dc.contributor.daisngid3320258-
dc.contributor.daisngid4588303-
dc.contributor.daisngid13190735-
dc.contributor.daisngid462854-
dc.contributor.daisngid641834-
dc.contributor.daisngid199914-
dc.contributor.daisngid214168-
dc.contributor.daisngid178539-
dc.contributor.daisngid795544-
dc.contributor.daisngid617657-
dc.identifier.investigatorRIDN-7551-2016-
dc.identifier.investigatorRIDH-1493-2015-
dc.identifier.investigatorRIDH-6075-2015-
dc.identifier.investigatorRIDNo ID-
dc.identifier.investigatorRIDNo ID-
dc.identifier.investigatorRIDNo ID-
dc.identifier.investigatorRIDNo ID-
dc.identifier.investigatorRIDNo ID-
dc.description.numberofpages10en_US
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Zadjali, F-
dc.contributor.wosstandardWOS:Santana-Farre, R-
dc.contributor.wosstandardWOS:Vesterlund, M-
dc.contributor.wosstandardWOS:Carow, B-
dc.contributor.wosstandardWOS:Mirecki-Garrido, M-
dc.contributor.wosstandardWOS:Hernandez-Hernandez, I-
dc.contributor.wosstandardWOS:Flodstrom-Tullberg, M-
dc.contributor.wosstandardWOS:Parini, P-
dc.contributor.wosstandardWOS:Rottenberg, M-
dc.contributor.wosstandardWOS:Norstedt, G-
dc.contributor.wosstandardWOS:Fernandez-Perez, L-
dc.contributor.wosstandardWOS:Flores-Morales, A-
dc.date.coverdateAgosto 2012en_US
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.sjr3,071-
dc.description.jcr5,704-
dc.description.sjrqQ1-
dc.description.jcrqQ1-
dc.description.scieSCIE-
item.grantfulltextnone-
item.fulltextSin texto completo-
crisitem.project.principalinvestigatorFernández Pérez, Leandro Francisco-
crisitem.author.deptGIR IUIBS: Medio Ambiente y Salud-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptGIR IUIBS: Farmacología Molecular y Traslacional-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Clínicas-
crisitem.author.deptGIR IUIBS: Farmacología Molecular y Traslacional-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.orcid0000-0003-0488-6307-
crisitem.author.orcid0000-0001-7174-7599-
crisitem.author.orcid0000-0001-7802-465X-
crisitem.author.orcid0000-0002-0828-8921-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameDe Mirecki Garrido, Mercedes-
crisitem.author.fullNameHernández Hernández,Irene-
crisitem.author.fullNameFernández Pérez, Leandro Francisco-
crisitem.author.fullNameFlores Morales,Amilcar-
Appears in Collections:Artículos
Show simple item record

SCOPUSTM   
Citations

59
checked on Nov 17, 2024

WEB OF SCIENCETM
Citations

60
checked on Nov 17, 2024

Page view(s)

55
checked on Jan 7, 2023

Google ScholarTM

Check

Altmetric


Share



Export metadata



Items in accedaCRIS are protected by copyright, with all rights reserved, unless otherwise indicated.