Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/87119
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampOliveira, Alexandre Gabarrapt_BR
dc.contributor.authorunicampSaad, Mário José Abdallapt_BR
dc.contributor.authorunicampTorello, Cristinae Okudapt_BR
dc.contributor.authorunicampQueiroz, Mary Luci de Souzapt_BR
dc.typeArtigopt_BR
dc.titleChlorella modulates insulin signaling pathway and prevents high-fat diet-induced insulin resistance in micept_BR
dc.contributor.authorAraujo, T.G.pt_BR
dc.contributor.authorVecina, J.F.pt_BR
dc.contributor.authorOliveira, A.G.pt_BR
dc.contributor.authorSaad, M.J.A.pt_BR
dc.contributor.authorBaggio, S.R.pt_BR
dc.contributor.authorTorello, C.O.pt_BR
dc.contributor.authorQueiroz, M.L.D.S.pt_BR
dc.subjectObesidadept_BR
dc.subjectResistência à insulinapt_BR
dc.subject.otherlanguageObesitypt_BR
dc.subject.otherlanguageInsulin resistancept_BR
dc.description.abstractAims The search for natural agents that minimize obesity-associated disorders is receiving special attention. In this regard, the present study aimed to evaluate the prophylactic effect of Chlorella vulgaris (CV) on body weight, lipid profile, blood glucose and insulin signaling in liver, skeletal muscle and adipose tissue of diet-induced obese mice. Main methods Balb/C mice were fed either with standard rodent chow diet or high-fat diet (HFD) and received concomitant treatment with CV for 12 consecutive weeks. Triglyceride, free fatty acid, total cholesterol and fractions of cholesterol were measured using commercial assay. Insulin and leptin levels were determined by enzyme-linked immunosorbent assay (ELISA). Insulin and glucose tolerance tests were performed. The expression and phosphorylation of IRβ, IRS-1 and Akt were determined by Western blot analyses. Key findings Herein we demonstrate for the first time in the literature that prevention by CV of high-fat diet-induced insulin resistance in obese mice, as shown by increased glucose and insulin tolerance, is in part due to the improvement in the insulin signaling pathway at its main target tissues, by increasing the phosphorylation levels of proteins such as IR, IRS-1 and Akt. In parallel, the lower phosphorylation levels of IRS-1ser307 were observed in obese mice. We also found that CV administration prevents high-fat diet-induced dyslipidemia by reducing triglyceride, cholesterol and free fatty acid levels. Significance We propose that the modulatory effect of CV treatment preventing the deleterious effects induced by high-fat diet is a good indicator for its use as a prophylactic-therapeutic agent against obesity-related complications. © 2013 Elsevier Inc. All rights reserved.en
dc.description.abstractAims the search for natural agents that minimize obesity-associated disorders is receiving special attention. In this regard, the present study aimed to evaluate the prophylactic effect of Chlorella vulgaris (CV) on body weight, lipid profile, blood glucose and insulin signaling in liver, skeletal muscle and adipose tissue of diet-induced obese mice. Main methods Balb/C mice were fed either with standard rodent chow diet or high-fat diet (HFD) and received concomitant treatment with CV for 12 consecutive weeks. Triglyceride, free fatty acid, total cholesterol and fractions of cholesterol were measured using commercial assay. Insulin and leptin levels were determined by enzyme-linked immunosorbent assay (ELISA). Insulin and glucose tolerance tests were performed. The expression and phosphorylation of IR?, IRS-1 and Akt were determined by Western blot analyses. Key findings Herein we demonstrate for the first time in the literature that prevention by CV of high-fat diet-induced insulin resistance in obese mice, as shown by increased glucose and insulin tolerance, is in part due to the improvement in the insulin signaling pathway at its main target tissues, by increasing the phosphorylation levels of proteins such as IR, IRS-1 and Akt. In parallel, the lower phosphorylation levels of IRS-1ser307 were observed in obese mice. We also found that CV administration prevents high-fat diet-induced dyslipidemia by reducing triglyceride, cholesterol and free fatty acid levels. Significance We propose that the modulatory effect of CV treatment preventing the deleterious effects induced by high-fat diet is a good indicator for its use as a prophylactic-therapeutic agent against obesity-related complicationspt
dc.relation.ispartofLife sciencespt_BR
dc.relation.ispartofabbreviationLife sci.pt_BR
dc.publisher.cityNew York, NYpt_BR
dc.publisher.countryEstados Unidospt_BR
dc.publisherHeadington Hill Hallpt_BR
dc.date.issued2014pt_BR
dc.identifier.citationLife Sciences. , v. 95, n. 1, p. 45 - 52, 2014.pt_BR
dc.language.isoengpt_BR
dc.description.volume95pt_BR
dc.description.issuenumber1pt_BR
dc.description.firstpage45pt_BR
dc.description.lastpage52pt_BR
dc.rightsfechadopt_BR
dc.sourceScopuspt_BR
dc.identifier.issn0024-3205pt_BR
dc.identifier.doi10.1016/j.lfs.2013.11.020pt_BR
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0024320513007467?via%3Dihubpt_BR
dc.date.available2015-06-25T17:56:47Z-
dc.date.available2015-11-26T14:47:17Z-
dc.date.accessioned2015-06-25T17:56:47Z-
dc.date.accessioned2015-11-26T14:47:17Z-
dc.description.provenanceMade available in DSpace on 2015-06-25T17:56:47Z (GMT). No. of bitstreams: 0 Previous issue date: 2014. Added 1 bitstream(s) on 2019-03-14T14:32:15Z : No. of bitstreams: 1 2-s2.0-84892374361.pdf: 834421 bytes, checksum: c6ca6f2bb6f6210397290cca31607ea1 (MD5) Bitstreams deleted on 2020-05-18T20:41:18Z: 2-s2.0-84892374361.pdf,. Added 1 bitstream(s) on 2020-05-19T14:31:10Z : No. of bitstreams: 1 2-s2.0-84892374361.pdf: 989237 bytes, checksum: 7cfd5b44d13ad7e076740f3e9896237c (MD5)en
dc.description.provenanceMade available in DSpace on 2015-11-26T14:47:17Z (GMT). No. of bitstreams: 0 Previous issue date: 2014en
dc.identifier.urihttp://www.repositorio.unicamp.br/handle/REPOSIP/87119-
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/87119-
dc.contributor.departmentInformação não localizadapt_BR
dc.contributor.departmentDepartamento de Clinica Médicapt_BR
dc.contributor.departmentInformação não localizadapt_BR
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.identifier.source2-s2.0-84892374361-
dc.creator.orcidInformação não localizadapt_BR
dc.creator.orcid0000-0003-4544-6105pt_BR
dc.creator.orcid0000-0002-1611-020Xpt_BR
dc.creator.orcidInformação não localizadapt_BR
dc.type.formArtigo originalpt_BR
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