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dc.contributor.CRUESPUniversidade Estadual de Campinaspt_BR
dc.typeArtigo de periódicopt_BR
dc.titleLow-Grade Hypothalamic Inflammation Leads to Defective Thermogenesis, Insulin Resistance, and Impaired Insulin Secretionpt_BR
dc.contributor.authorArruda, APpt_BR
dc.contributor.authorMilanski, Mpt_BR
dc.contributor.authorCoope, Apt_BR
dc.contributor.authorTorsoni, ASpt_BR
dc.contributor.authorRopelle, Ept_BR
dc.contributor.authorCarvalho, DPpt_BR
dc.contributor.authorCarvalheira, JBpt_BR
dc.contributor.authorVelloso, LApt_BR
unicamp.author.emaillavelloso.unicamp@gmail.compt_BR
unicamp.authorVelloso, Licio A. Univ Estadual Campinas, Dept Internal Med, Fac Med Sci, BR-13084761 Campinas, SP, Brazilpt_BR
unicamp.authorArruda, Ana Paula Milanski, Marciane Coope, Andressa Torsoni, Adriana S. Velloso, Licio A. Univ Estadual Campinas, Lab Cell Signaling, BR-13084761 Campinas, SP, Brazilpt_BR
unicamp.authorCarvalho, Denise P. Univ Fed Rio de Janeiro, Dept Endocrinol, Rio De Janeiro, Brazilpt_BR
dc.subject.wosNecrosis-factor-alphapt_BR
dc.subject.wosBrown Adipose-tissuept_BR
dc.subject.wosDiet-induced Obesitypt_BR
dc.subject.wosSignaling Pathwayspt_BR
dc.subject.wosFood-intakept_BR
dc.subject.wosTnf-alphapt_BR
dc.subject.wosMechanismspt_BR
dc.subject.wosLeptinpt_BR
dc.subject.wosActivationpt_BR
dc.subject.wosExpressionpt_BR
dc.description.abstractHypothalamic inflammation is present in animal models of obesity, and the intracere broventricular injection of TNF alpha can reproduce a number of features of the hypothalamus of obese animals. Because obesity is a risk factor for type 2 diabetes (DM2) we hypothesized that, by inducing hypothalamic inflammation, we could reproduce some clinical features of DM2. Lean Wistar rats and TNF receptor 1-knockout mice were employed to determine the effects of hypothalamic actions of TNF alpha on thermogenesis and metabolic parameters. Signal transduction and protein expression were evaluated by immunoblot and real-time PCR. Thermogenesis was evaluated in living rats, and respirometry was determined in isolated muscle fiber. In Wistar rats, hypothalamic TNF alpha blunts the anorexigenic effect of leptin, which is accompanied by reduced leptin signaling and increased expression of suppressor of cytokine signaling 3. In addition, hypothalamic TNF alpha reduces O(2) consumption and the expression of thermogenic proteins in brown adipose tissue and skeletal muscle. Furthermore, hypothalamic inflammation increases base-line plasma insulin and insulin secretion by isolated pancreatic islets, which is accompanied by an impaired insulin signal transduction in liver and skeletal muscle. Hypothalamic inflammation induced by stearic acid also reduces O(2) consumption and blunts peripheral insulin signal transduction. The use of intracere broventricular infliximab restores O(2) consumption in obese rats, whereas TNF receptor 1-knockout mice are protected from diet-induced reduced thermogenesis and defective insulin signal transduction. Thus, low-grade inflammation of the hypothalamus is sufficient to induce changes in a number of parameters commonly impaired in obesity and DM2, and TNF alpha is an important mediator of this process. (Endocrinology 152: 1314-1326, 2011)pt
dc.description.noteo TEXTO COMPLETO DESTE ARTIGO, ESTARÁ DISPONÍVEL À PARTIR DE AGOSTO DE 2015.pt
dc.relation.ispartofEndocrinologypt_BR
dc.relation.ispartofabbreviationEndocrinologypt_BR
dc.publisher.cityChevy Chasept_BR
dc.publisher.countryEUApt_BR
dc.publisherEndocrine Socpt_BR
dc.date.issued2011pt_BR
dc.date.monthofcirculationAPRpt_BR
dc.identifier.citationEndocrinology. Endocrine Soc, v. 152, n. 4, n. 1314, n. 1326, 2011.pt_BR
dc.language.isoenpt_BR
dc.description.volume152pt_BR
dc.description.issuenumber4pt_BR
dc.description.firstpage1314pt_BR
dc.description.lastpage1326pt_BR
dc.rightsembargopt_BR
dc.sourceWeb of Sciencept_BR
dc.identifier.issn0013-7227pt_BR
dc.identifier.wosidWOS:000288696300014pt_BR
dc.identifier.doi10.1210/en.2010-0659pt_BR
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
dc.description.sponsorship1Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorship1Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt_BR
dc.date.available2014-07-30T13:39:11Z
dc.date.available2015-11-26T16:32:07Z-
dc.date.accessioned2014-07-30T13:39:11Z
dc.date.accessioned2015-11-26T16:32:07Z-
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dc.description.provenanceMade available in DSpace on 2015-11-26T16:32:07Z (GMT). No. of bitstreams: 2 WOS000288696300014.pdf: 2375582 bytes, checksum: 48d02746802b1e34aa643b32eb5c6b00 (MD5) WOS000288696300014.pdf.txt: 49259 bytes, checksum: 5c0f968381cab26d3f012085eb55d798 (MD5) Previous issue date: 2011en
dc.identifier.urihttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/52830
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/52830-
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