Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/348806
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampMilanski, Marciane-
dc.contributor.authorunicampRomanatto, Talita-
dc.contributor.authorunicampSolon, Carina Silva-
dc.contributor.authorunicampCoope, Andressa-
dc.contributor.authorunicampAlberici, Luciane Carla-
dc.contributor.authorunicampFestuccia, William Tadeu Lara-
dc.contributor.authorunicampRopelle, Eduardo Rochete-
dc.contributor.authorunicampCarvalheira, José Barreto Campello-
dc.contributor.authorunicampVercesi, Anibal Eugenio-
dc.contributor.authorunicampVelloso, Licio Augusto-
dc.typeArtigopt_BR
dc.titleHypothalamic actions of tumor necrosis factor α provide the thermogenic core for the wastage syndrome in cachexiapt_BR
dc.contributor.authorArruda, Ana Paula-
dc.contributor.authorMilanski, Marciane-
dc.contributor.authorRomanatto, Talita-
dc.contributor.authorSolon, Carina-
dc.contributor.authorCoope, Andressa-
dc.contributor.authorAlberici, Luciane C.-
dc.contributor.authorFestuccia, William T.-
dc.contributor.authorHirabara, Sandro M.-
dc.contributor.authorRopelle, Eduardo-
dc.contributor.authorCuri, Rui-
dc.contributor.authorCarvalheira, José B.-
dc.contributor.authorVercesi, Aníbal E.-
dc.contributor.authorVelloso, Licio A.-
dc.subjectCitocinaspt_BR
dc.subject.otherlanguageCytokinespt_BR
dc.description.abstractTNFα is an important mediator of catabolism in cachexia. Most of its effects have been characterized in peripheral tissues, such as skeletal muscle and fat. However, by acting directly in the hypothalamus, TNFα can activate thermogenesis and modulate food intake. Here we show that high concentration TNFα in the hypothalamus leads to increased O2 consumption/CO2 production, increased body temperature, and reduced caloric intake, resulting in loss of body mass. Most of the thermogenic response is produced by β3-adrenergic signaling to the brown adipose tissue (BAT), leading to increased BAT relative mass, reduction in BAT lipid quantity, and increased BAT mitochondria density. The expression of proteins involved in BAT thermogenesis, such as β3-adrenergic receptor, peroxisomal proliferator-activated receptor-γ coactivator-1α, and uncoupling protein-1, are increased. In the hypothalamus, TNFα produces reductions in neuropeptide Y, agouti gene-related peptide, proopiomelanocortin, and melanin-concentrating hormone, and increases CRH and TRH. The activity of the AMP-activated protein kinase signaling pathway is also decreased in the hypothalamus of TNFα-treated rats. Upon intracerebroventricular infliximab treatment, tumor-bearing and septic rats present a significantly increased survival. In addition, the systemic inhibition of β3-adrenergic signaling results in a reduced body mass loss and increased survival in septic rats. These data suggest hypothalamic TNFα action to be important mediator of the wastage syndrome in cachexiapt_BR
dc.relation.ispartofEndocrinologypt_BR
dc.relation.ispartofabbreviationEndocrinol.pt_BR
dc.publisher.cityCary, NCpt_BR
dc.publisher.countryEstados Unidospt_BR
dc.publisherOxford University Presspt_BR
dc.date.issued2010-
dc.date.monthofcirculationFeb.pt_BR
dc.language.isoengpt_BR
dc.description.volume151pt_BR
dc.description.issuenumber2pt_BR
dc.description.firstpage683pt_BR
dc.description.lastpage694pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn0013-7227pt_BR
dc.identifier.eissn1945-7170pt_BR
dc.identifier.doi10.1210/en.2009-0865pt_BR
dc.identifier.urlhttps://academic.oup.com/endo/article/151/2/683/2456462pt_BR
dc.description.sponsorshipCONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQpt_BR
dc.description.sponsordocumentnumberNão tempt_BR
dc.description.sponsordocumentnumberNão tempt_BR
dc.date.available2020-09-08T11:52:45Z-
dc.date.accessioned2020-09-08T11:52:45Z-
dc.description.provenanceSubmitted by Susilene Barbosa da Silva (susilene@unicamp.br) on 2020-09-08T11:52:45Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-01-04T15:12:48Z : No. of bitstreams: 1 000273948600027.pdf: 677983 bytes, checksum: 9350367745f698e8f08eae91aeea3ef1 (MD5)en
dc.description.provenanceMade available in DSpace on 2020-09-08T11:52:45Z (GMT). No. of bitstreams: 0 Previous issue date: 2010en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/348806-
dc.contributor.departmentSem informaçãopt_BR
dc.contributor.departmentSem informaçãopt_BR
dc.contributor.departmentSem informaçãopt_BR
dc.contributor.departmentSem informaçãopt_BR
dc.contributor.departmentSem informaçãopt_BR
dc.contributor.departmentSem informaçãopt_BR
dc.contributor.departmentSem informaçãopt_BR
dc.contributor.departmentSem informaçãopt_BR
dc.contributor.departmentDepartamento de Patologia Clínicapt_BR
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.subject.keywordGrowth Factorspt_BR
dc.identifier.source000273948600027pt_BR
dc.creator.orcid0000-0002-6322-5368pt_BR
dc.creator.orcidSem informaçãopt_BR
dc.creator.orcidSem informaçãopt_BR
dc.creator.orcidSem informaçãopt_BR
dc.creator.orcidSem informaçãopt_BR
dc.creator.orcid0000-0003-4769-0806pt_BR
dc.creator.orcid0000-0003-1655-9557pt_BR
dc.creator.orcid0000-0002-0136-0943pt_BR
dc.creator.orcid0000-0002-0504-5676pt_BR
dc.creator.orcid0000-0002-4806-7218pt_BR
dc.type.formArtigopt_BR
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