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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.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.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.publisherAmer Diabetes Assocpt_BR
dc.identifier.citationDiabetes. Amer Diabetes Assoc, v. 61, n. 6, n. 1455, n. 1462, 2012.pt_BR
dc.sourceWeb of Sciencept_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.description.provenanceMade available in DSpace on 2014-08-01T18:32:55Z (GMT). No. of bitstreams: 0 Previous issue date: 2012en
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