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dc.contributor.CRUESPUniversidade Estadual de Campinaspt_BR
dc.typeArtigo de periódicopt_BR
dc.titleInhibition of Hypothalamic Inflammation Reverses Diet-Induced Insulin Resistance in the Liverpt_BR
dc.contributor.authorMilanski, Mpt_BR
dc.contributor.authorArruda, APpt_BR
dc.contributor.authorCoope, Apt_BR
dc.contributor.authorIgnacio-Souza, LMpt_BR
dc.contributor.authorNunez, CEpt_BR
dc.contributor.authorRoman, EApt_BR
dc.contributor.authorRomanatto, Tpt_BR
dc.contributor.authorPascoal, LBpt_BR
dc.contributor.authorCaricilli, AMpt_BR
dc.contributor.authorTorsoni, MApt_BR
dc.contributor.authorPrada, POpt_BR
dc.contributor.authorSaad, MJpt_BR
dc.contributor.authorVelloso, LApt_BR
unicamp.author.emaillavelloso.unicamp@gmail.compt_BR
unicamp.authorMilanski, Marciane Arruda, Ana P. Coope, Andressa Ignacio-Souza, Leticia M. Nunez, Carla E. Roman, Erika A. Romanatto, Talita Pascoal, Livia B. Torsoni, Marcio A. Velloso, Licio A. Univ Estadual Campinas, Lab Cell Signaling, Campinas, Brazilpt_BR
unicamp.authorMilanski, Marciane Torsoni, Marcio A. Prada, Patricia O. Univ Estadual Campinas, Fac Sci Appl, Campinas, Brazilpt_BR
unicamp.authorCaricilli, Andrea M. Saad, Mario J. Univ Estadual Campinas, Dept Internal Med, Campinas, Brazilpt_BR
dc.subject.wosHepatic Glucose-productionpt_BR
dc.subject.wosInduced Obesitypt_BR
dc.subject.wosMicept_BR
dc.subject.wosLeptinpt_BR
dc.subject.wosPathogenesispt_BR
dc.subject.wosSensitivitypt_BR
dc.subject.wosMetabolismpt_BR
dc.subject.wosMinireviewpt_BR
dc.subject.wosDiseasept_BR
dc.subject.wosStresspt_BR
dc.description.abstractDefective liver gluconeogenesis is the main mechanism leading to fasting hyperglycemia in type 2 diabetes, and, in concert with steatosis, it is the hallmark of hepatic insulin resistance. Experimental obesity results, at least in part, from hypothalamic inflammation, which leads to leptin resistance and defective regulation of energy homeostasis. Pharmacological or genetic disruption of hypothalamic inflammation restores leptin sensitivity and reduces adiposity. Here, we evaluate the effect of a hypothalamic anti-inflammatory approach to regulating hepatic responsiveness to insulin. Obese rodents were treated by intracerebroventricular injections, with immunoneutralizing antibodies against Toll-like receptor (TLR) 4 or tumor necrosis factor (TNF)alpha, and insulin signal transduction, hepatic steatosis, and gluconeogenesis were evaluated. The inhibition of either TLR4 or TNF alpha reduced hypothalamic inflammation, which was accompanied by the reduction of hypothalamic resistance to leptin and improved insulin signal transduction in the liver. This was accompanied by reduced liver steatosis and reduced hepatic expression of markers of steatosis. Furthermore, the inhibition of hypothalamic inflammation restored defective liver glucose production. All these beneficial effects were abrogated by vagotomy. Thus, the inhibition of hypothalamic inflammation in obesity results in improved hepatic insulin signal transduction, leading to reduced steatosis and reduced gluconeogenesis. All these effects are mediated by parasympathetic signals delivered by the vagus nerve. Diabetes 61:1455-1462, 2012pt
dc.relation.ispartofDiabetespt_BR
dc.relation.ispartofabbreviationDiabetespt_BR
dc.publisher.cityAlexandriapt_BR
dc.publisher.countryEUApt_BR
dc.publisherAmer Diabetes Assocpt_BR
dc.date.issued2012pt_BR
dc.date.monthofcirculationJUNpt_BR
dc.identifier.citationDiabetes. Amer Diabetes Assoc, v. 61, n. 6, n. 1455, n. 1462, 2012.pt_BR
dc.language.isoenpt_BR
dc.description.volume61pt_BR
dc.description.issuenumber6pt_BR
dc.description.firstpage1455pt_BR
dc.description.lastpage1462pt_BR
dc.rightsfechadopt_BR
dc.sourceWeb of Sciencept_BR
dc.identifier.issn0012-1797pt_BR
dc.identifier.wosidWOS:000304490100022pt_BR
dc.identifier.doi10.2337/db11-0390pt_BR
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.description.sponsorship1Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt_BR
dc.date.available2014-08-01T18:32:55Z
dc.date.available2015-11-26T17:59:54Z-
dc.date.accessioned2014-08-01T18:32:55Z
dc.date.accessioned2015-11-26T17:59:54Z-
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dc.identifier.urihttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/80585
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/80585-
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