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dc.contributor.authorNascimento, Andre F. [UNESP]
dc.contributor.authorLuvizotto, Renata A. M. [UNESP]
dc.contributor.authorLeopoldo, Andre S. [UNESP]
dc.contributor.authorLima-Leopoldo, Ana P. [UNESP]
dc.contributor.authorSeiva, Fabio R. [UNESP]
dc.contributor.authorJustulin, Luis A. [UNESP]
dc.contributor.authorSilva, Maeli Dal Pai [UNESP]
dc.contributor.authorOkoshi, Katashi [UNESP]
dc.contributor.authorWang, Xiang-Dong
dc.contributor.authorCicogna, Antonio Carlos [UNESP]
dc.date.accessioned2014-05-20T13:33:53Z
dc.date.available2014-05-20T13:33:53Z
dc.date.issued2011-06-06
dc.identifierhttp://dx.doi.org/10.1016/j.lfs.2011.03.015
dc.identifier.citationLife Sciences. Oxford: Pergamon-Elsevier B.V. Ltd, v. 88, n. 23-24, p. 1031-1038, 2011.
dc.identifier.issn0024-3205
dc.identifier.urihttp://hdl.handle.net/11449/11595
dc.description.abstractAims: Leptin resistance has been associated with cardiac lipotoxicity; however, whether leptin resistance is a risk factor associated with cardiac lipotoxicity at different time points in diet-induced obesity is unclear. The objective of this study was to evaluate this relationship.Main methods: Male Wistar rats were fed a normal chow diet (12% from fat) or a high-fat diet (49% from fat) for 15 and 45 weeks, respectively. The adiposity index, body weight and co-morbidities were evaluated. Heart lipotoxicity was assessed by analyzing cardiac function and morphological changes as well as cardiac triglyceride, ceramide and lipid hydroperoxide accumulations. Cardiac apoptosis was examined using the TUNEL method. Leptin function was determined by examining plasma leptin levels, cardiac leptin receptors (OB-R) and related phosphorylations of AMP-activated kinase protein (AMPK) and Acetyl CoA carboxylase (ACC).Key findings: The diet-induced obesity was characterized by an elevated adiposity index, body weight and leptin levels at both 15 and 45 weeks. There was no difference between groups in the cardiac triglyceride or lipid hydroperoxide levels. Interestingly, ceramide levels decreased in obese animals in both experimental periods. The cardiac morphological and functional parameters were not altered. Although down-regulation of OB-R has occurred in chronic obesity, it did not adversely affect AMPK or ACC phosphorylation.Significance: The development of obesity via long-term feeding of a high-fat diet to rats does not result in cardiac lipotoxicity but promotes the down-regulation of OB-R. However, this does not result in altered levels of AMPK or ACC phosphotylations in this animal model. (C) 2011 Elsevier B.V. All rights reserved.en
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipUS Department of Agriculture
dc.format.extent1031-1038
dc.language.isoeng
dc.publisherPergamon-Elsevier B.V. Ltd
dc.relation.ispartofLife Sciences
dc.sourceWeb of Science
dc.subjectCardiac lipotoxicityen
dc.subjectCardiac leptin receptoren
dc.subjectDiet-induced obesityen
dc.subjectHigh-fat dieten
dc.titleLong-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicityen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderPergamon-Elsevier B.V. Ltd
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionTufts Univ
dc.description.affiliationSão Paulo State Univ UNESP, Botucatu Sch Med, Dept Clin Med, Botucatu, SP, Brazil
dc.description.affiliationSão Paulo State Univ UNESP, Inst Biosci, Dept Morphol, Botucatu, SP, Brazil
dc.description.affiliationTufts Univ, Jean Mayer USDA, Human Nutr Res Ctr Aging, Boston, MA 02111 USA
dc.description.affiliationTufts Univ, Dept Nutr Sci, Gerald J & Dorothy R Friedman Sch Nutr Sci & Poli, Boston, MA 02111 USA
dc.description.affiliationUnespSão Paulo State Univ UNESP, Botucatu Sch Med, Dept Clin Med, Botucatu, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ UNESP, Inst Biosci, Dept Morphol, Botucatu, SP, Brazil
dc.identifier.doi10.1016/j.lfs.2011.03.015
dc.identifier.wosWOS:000291299300005
dc.rights.accessRightsAcesso aberto
dc.description.sponsorshipIdCNPq: 471256/2007-2
dc.description.sponsorshipIdUS Department of Agriculture: 1950-51000-064S
unesp.campusUniversidade Estadual Paulista (UNESP), Instituto de Biociências, Botucatupt
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Medicina, Botucatupt
dc.identifier.fileWOS000291299300005.pdf
dc.identifier.lattes1590971576309420
dc.identifier.lattes9418970103564137
unesp.author.lattes1590971576309420
unesp.author.lattes9418970103564137[10]
unesp.author.orcid0000-0002-7461-8773[5]
unesp.author.orcid0000-0001-6142-3515[6]
unesp.author.orcid0000-0001-8980-8839[8]
unesp.author.orcid0000-0002-4402-6523[10]
dc.relation.ispartofjcr3.234
dc.relation.ispartofsjr1,071
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