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dc.contributor.authorRomanatto, Talita
dc.contributor.authorCesquini, Maristela
dc.contributor.authorAmaral, Maria E.
dc.contributor.authorRoman, Erika A.
dc.contributor.authorMoraes, Juliana C.
dc.contributor.authorTorsoni, Marcio A.
dc.contributor.authorCruz-Neto, Ariovaldo P.
dc.contributor.authorVelloso, Licio A.
dc.date.accessioned2014-02-26T17:29:43Z
dc.date.accessioned2014-05-20T13:59:09Z
dc.date.available2014-02-26T17:29:43Z
dc.date.available2014-05-20T13:59:09Z
dc.date.issued2007-05-01
dc.identifierhttp://dx.doi.org/10.1016/j.peptides.2007.03.006
dc.identifier.citationPeptides. New York: Elsevier B.V., v. 28, n. 5, p. 1050-1058, 2007.
dc.identifier.issn0196-9781
dc.identifier.urihttp://hdl.handle.net/11449/21030
dc.description.abstractActing in the hypothalamus, tumor necrosis factor-alpha (TNF-alpha) produces a potent anorexigenic effect. However, the molecular mechanisms involved in this phenomenon are poorly characterized. In this study, we investigate the capacity of TNF-alpha to activate signal transduction in the hypothalamus through elements of the pathways employed by the anorexigenic hormones insulin and leptin. High dose TNF-a promotes a reduction of 25% in 12 h food intake, which is an inhibitory effect that is marginally inferior to that produced by insulin and leptin. In addition, high dose TNF-a increases body temperature and respiratory quotient, effects not reproduced by insulin or leptin. TNF-alpha, predominantly at the high dose, is also capable of activating canonical pro-inflammatory signal transduction in the hypothalamus, inducing JNK, p38, and NF kappa B, which results in the transcription of early responsive genes and expression of proteins of the SOCS family. Also, TNF-a activates signal transduction through JAK-2 and STAT-3, but does not activate signal transduction. through early and intermediary elements of the insulin/leptin signaling pathways such as IRS-2, Akt, ERK and FOXO1. When co-injected with insulin or leptin, TNF-a, at both high and low doses, partially impairs signal transduction through IRS-2, Akt, ERK and FOXO1 but not through JAK-2 and STAT-3. This effect is accompanied by the partial inhibition of the anorexigenic effects of insulin and leptin, when the low, but not the high dose of TNF-alpha is employed. In conclusion, TNF-alpha, on a dose-dependent way, modulates insulin and leptin signaling and action in the hypothalamus. (c) Published by Elsevier B.V.en
dc.format.extent1050-1058
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofPeptides
dc.sourceWeb of Science
dc.subjectfeedingpt
dc.subjectinsulinpt
dc.subjectleptinpt
dc.subjectcytokinept
dc.subjectinflammationpt
dc.titleTNF-alpha acts in the hypothalamus inhibiting food intake and increasing the respiratory quotient - Effects on leptin and insulin signaling pathwaysen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.description.affiliationUniv Estadual Campinas, FCM, DCM, Dept Internal Med, BR-13084970 Campinas, SP, Brazil
dc.description.affiliationUniv Estadual Paulista, Dept Zool, Rio Claro, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, Dept Zool, Rio Claro, Brazil
dc.identifier.doi10.1016/j.peptides.2007.03.006
dc.identifier.wosWOS:000246934900013
dc.rights.accessRightsAcesso restrito
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Rio Claropt
unesp.author.lattes5758081094133626[7]
unesp.author.orcid0000-0001-5128-2202[3]
unesp.author.orcid0000-0001-5270-7276[7]
dc.relation.ispartofjcr2.851
dc.relation.ispartofsjr1,001
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