dc.creatorVitto, MF
dc.creatorLuz, G
dc.creatorLuciano, TF
dc.creatorMarques, SO
dc.creatorSouza, DR
dc.creatorPinho, RA
dc.creatorLira, FS
dc.creatorCintra, DE
dc.creatorDe Souza, CT
dc.date2012
dc.dateNOV
dc.date2014-08-01T18:29:58Z
dc.date2015-11-26T17:08:20Z
dc.date2014-08-01T18:29:58Z
dc.date2015-11-26T17:08:20Z
dc.date.accessioned2018-03-28T23:56:58Z
dc.date.available2018-03-28T23:56:58Z
dc.identifierHormone And Metabolic Research. Georg Thieme Verlag Kg, v. 44, n. 12, n. 885, n. 890, 2012.
dc.identifier0018-5043
dc.identifierWOS:000311138800003
dc.identifier10.1055/s-0032-1321819
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/79790
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/79790
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1280338
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionThe literature has associated hepatic insulin action with NAFLD. In this sense, treatments to revert steatosis and improve hepatic insulin action become important. Our group has demonstrated that inhibition of Sterol Regulatory Element Binding Proteins-1c (SREBP-1c) reverses hepatic steatosis. However, insulin signals after NAFLD reversion require better investigation. Thus, in this study, we investigated if the reversal of NAFLD by SREBP-1c inhibitor results in improvement in the hepatic insulin signal in obesity mice. After installation/achievement of diet-induced obesity and insulin resistance, Swiss mice were divided into 3 groups: i) Lean, ii) D-IHS, diet-induced hepatic steatosis [no treatment with antisense oligonucleotide (ASO)], and iii) RD-IHS, reversion of diet-induced hepatic steatosis (treated with ASO). The mice were treated with ASO SREBP-1c as previously described by our group. After ASO treatment, one set of animals was anesthetized and used for in vivo test, and another mice set was anesthetized and used for histology and Western blot analysis. Reversion of diet-induced hepatic steatosis did not change blood glucose, glucose decay constant (k(ITT)), body weight, or serum insulin levels. In addition, results showed that the protocol did not improve insulin pathway signaling, as confirmed by the absence of changes in IR, IRS1, Akt and Foxo1 phosphorylation in hepatic tissue. In parallel, no alterations were observed in proinflammatory molecules. Thus, our results suggest that the inhibition of SREBP-1c reverts steatosis, but without improving insulin hepatic resistance.
dc.description44
dc.description12
dc.description885
dc.description890
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundacao de Amparo a Pesquisa do Estado de Santa Catarina (FAPESC)
dc.descriptionUniversidade do Extremo Sul Catarinense (UNESC)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.languageen
dc.publisherGeorg Thieme Verlag Kg
dc.publisherStuttgart
dc.publisherAlemanha
dc.relationHormone And Metabolic Research
dc.relationHorm. Metab. Res.
dc.rightsaberto
dc.sourceWeb of Science
dc.subjectSREBP-1c
dc.subjectsteatosis
dc.subjectinsulin resistance
dc.subjectinflammation
dc.subjectFatty Liver-disease
dc.subjectNecrosis-factor-alpha
dc.subjectKappa-b Activation
dc.subjectProtein-kinase-c
dc.subjectPhosphoinositide 3-kinase
dc.subjectResistance
dc.subjectExpression
dc.subjectPathway
dc.subjectInterleukin-10
dc.subjectAdipocytes
dc.titleReversion of Steatosis by SREBP-1c Antisense Oligonucleotide did not Improve Hepatic Insulin Action in Diet-induced Obesity Mice
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución