Disfunção miocárdica e alterações no trânsito de cálcio intracelular em ratos obesos

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dc.contributor.authorLeopoldo, Ana Paula Lima
dc.contributor.authorAndré S. Leopoldo [UNESP]
dc.contributor.authorSugizaki, Mario Mateus
dc.contributor.authorBruno, Alessandro
dc.contributor.authorNascimento, André Ferreira do
dc.contributor.authorLuvizotto, R A M
dc.contributor.authorOliveira Júnior, A S
dc.contributor.authorCastardeli, Edson
dc.contributor.authorPadovani, Carlos Roberto
dc.contributor.authorCicogna, Antonio Carlos [UNESP]
dc.contributor.institutionUniversidade Federal do Espírito Santo (UFES)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Federal do Mato Grosso (UFMT)
dc.date.accessioned2016-04-01T18:42:48Z
dc.date.available2016-04-01T18:42:48Z
dc.date.issued2011
dc.description.abstractAbstract Background: Several mechanisms have been proposed to contribute to cardiac dysfunction in obesity models, such as alterations in calcium (Ca2+) handling proteins and β-adrenergic receptors. Nevertheless, the role of these factors in the development of myocardial dysfunction induced by obesity is still not clear. Objective: The purpose of this study was to investigate whether obesity induced by hypercaloric diets results in cardiac dysfunction. Furthermore, it was evaluated whether this functional abnormality in obese rats is related to abnormal Ca2+ handling and the β-adrenoceptor system. Methods: Male 30-day-old Wistar rats were fed with standard food (C) and a cycle of five hypercaloric diets (Ob) for 15 weeks. Obesity was defined as increases in body fat percentage in rats. Cardiac function was evaluated by isolated analysis of the left ventricle papillary muscle under basal conditions and after inotropic and lusitropic maneuvers. Results: Compared with the control group, the obese rats had increased body fat and glucose intolerance. The muscles of obese rats developed similar baseline data, but the myocardial responsiveness to post-rest contraction stimulus and increased extracellular Ca2+ were compromised. There were no changes in cardiac function between groups after β-adrenergic stimulation. Conclusion: Obesity promotes cardiac dysfunction related to changes in intracellular Ca2+ handling. This functional damage is probably caused by reduced cardiac sarcoplasmic reticulum Ca2+ ATPase (SERCA2) activation via Ca2+ calmodulin kinase. (Arq Bras Cardiol 2011; 97(3) : 232-240).en
dc.description.affiliationDepartamento de Desportos, Centro de Educação Física e Desportos, UFES - Universidade Federal do Espírito Santo
dc.description.affiliationInstituto de Ciências da Saúde, UFMT - Universidade Federal de Mato Grosso
dc.description.affiliationUnespUniversidade Estadual Paulista Júlio de Mesquita Filho, Departamento de Clínica Médica, Faculdade de Medicina de Botucatu, Botucatu, Distrito de Rubião Júnior, s/nº, CEP 18600-000, SP, Brasil
dc.format.extent232-240
dc.identifierhttp://www.scielo.br/scielo.php?pid=S0066-782X2011005000061&script=sci_arttext
dc.identifier.citationArquivos Brasileiros de Cardiologia, v. 13, n. x, p. x-xx, 2011.
dc.identifier.fileISSN0066-782X-2011-13-232-240.pdf
dc.identifier.issn0066-782X
dc.identifier.lattes9418970103564137
dc.identifier.urihttp://hdl.handle.net/11449/136828
dc.language.isopor
dc.relation.ispartofArquivos Brasileiros de Cardiologia
dc.relation.ispartofjcr1.318
dc.rights.accessRightsAcesso aberto
dc.sourceCurrículo Lattes
dc.subjectMyocardial dysfunctionen
dc.subjectRatsen
dc.subjectObesityen
dc.subjectCalcium elevationen
dc.subjectReceptorsen
dc.subjectAdrenergicen
dc.subjectBetaen
dc.subjectDisfunção ventricularpt
dc.subjectRatospt
dc.subjectObesidadept
dc.subjectHipercalcemiapt
dc.subjectReceptores beta-adrenérgicospt
dc.titleDisfunção miocárdica e alterações no trânsito de cálcio intracelular em ratos obesospt
dc.title.alternativeMyocardial dysfunction and abnormalities in intracellular calcium handling in obese ratsen
dc.typeArtigo
unesp.author.lattes9418970103564137[10]
unesp.author.lattes8727897080522289[9]
unesp.author.orcid0000-0002-4402-6523[10]
unesp.author.orcid0000-0002-7719-9682[9]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt
unesp.departmentClínica Médicapt

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