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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampLeite, Nayara de Carvalho-
dc.typeArtigopt_BR
dc.titleSplenectomy attenuates obesity and decreases insulin hypersecretion in hypothalamic obese ratspt_BR
dc.contributor.authorLeite, Nayara de Carvalho-
dc.contributor.authorMontes, Elisangela Gueiber-
dc.contributor.authorFisher, Stefani Valéria-
dc.contributor.authorCancian, Cláudia Regina Capriglioni-
dc.contributor.authorOliveira, Júlio Cezar de-
dc.contributor.authorMartins-Pinge, Marli Cardoso-
dc.contributor.authorKanunfre, Carla Cristine-
dc.contributor.authorSouza, Kleber Luiz Araujo-
dc.contributor.authorGrassiolli, Sabrina-
dc.subjectObesidadept_BR
dc.subject.otherlanguageObesitypt_BR
dc.description.abstractObesity-induced abnormalities, such as insulin resistance, dyslipidemia and hypertension, are frequently correlated with low-grade inflammation, a process that may depend on normal spleen function. This study investigated the role of the spleen in the obesity induced by monosodium glutamate (MSG) treatment. MSG-obese and lean control (CON) rats were subjected to splenectomy (SPL) or non-operated (NO). MSG-NO rats presented a high adipose tissue content, insulin resistance, dyslipidemia and islet hypersecretion, accompanied by hypertrophy of both pancreatic islets and adipocytes when compared with CON-NO rats. In addition, changes in nitric oxide response were found in islets from the MSG-NO group without associated alterations in inducible nitric oxide synthase (iNOS) or IL1β expression. MSG-NO also presented increased leukocyte counts and augmented LPS-induced nitric oxide production in macrophages. Splenectomy of MSG-obese animals decreased insulin hypersecretion, normalized the nitric oxide response in the pancreatic islets, improved insulin sensitivity and reduced hypertrophy of both adipocytes and islets, when compared with MSG-NO rats. Results show that splenectomy attenuates the progression of the obesity modulating pancreas functions in MSG-obese ratspt_BR
dc.relation.ispartofMetabolism: clinical and experimentalpt_BR
dc.relation.ispartofabbreviationMetabolismpt_BR
dc.publisher.cityPhiladelphia, PApt_BR
dc.publisher.countryEstados Unidospt_BR
dc.publisherElsevierpt_BR
dc.date.issued2015-
dc.date.monthofcirculationSept.pt_BR
dc.language.isoengpt_BR
dc.description.volume64pt_BR
dc.description.issuenumber9pt_BR
dc.description.firstpage1122pt_BR
dc.description.lastpage1133pt_BR
dc.rightsFechadopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn0026-0495pt_BR
dc.identifier.eissn1532-8600pt_BR
dc.identifier.doi10.1016/j.metabol.2015.05.003pt_BR
dc.identifier.urlhttps://www.metabolismjournal.com/article/S0026-0495(15)00135-3/pt_BR
dc.date.available2021-01-28T15:20:05Z-
dc.date.accessioned2021-01-28T15:20:05Z-
dc.description.provenanceSubmitted by Susilene Barbosa da Silva (susilene@unicamp.br) on 2021-01-28T15:20:05Z No. of bitstreams: 0. Added 1 bitstream(s) on 2021-02-26T13:23:19Z : No. of bitstreams: 1 000360102600023.pdf: 1461961 bytes, checksum: 0f8fa1d8ebc2abb94324555ed12dbb70 (MD5)en
dc.description.provenanceMade available in DSpace on 2021-01-28T15:20:05Z (GMT). No. of bitstreams: 0 Previous issue date: 2015en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/354877-
dc.contributor.departmentSem informaçãopt_BR
dc.contributor.unidadeInstituto de Biologiapt_BR
dc.identifier.source000360102600023pt_BR
dc.creator.orcidSem informaçãopt_BR
dc.type.formArtigopt_BR
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