Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway

Detalhes bibliográficos
Autor(a) principal: Campos, Dijon Henrique Salomé De
Data de Publicação: 2014
Outros Autores: Leopoldo, André Soares, Lima-leopoldo, Ana Paula, Nascimento, André Ferreira Do, Oliveira-junior, Silvio Assis De, Silva, Danielle Cristina Tomaz Da, Sugizaki, Mario Mateus, Padovani, Carlos Roberto [UNESP], Cicogna, Antonio Carlos [UNESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.5935/abc.20140135
http://hdl.handle.net/11449/114472
Resumo: Background: Obesity is defined by excessive accumulation of body fat relative to lean tissue. Studies during the last few years indicate that cardiac function in obese animals may be preserved, increased or diminished. Objective: Study the energy balance of the myocardium with the hypothesis that the increase in fatty acid oxidation and reduced glucose leads to cardiac dysfunction in obesity. Methods: 30-day-old male Wistar rats were fed standard and hypercaloric diet for 30 weeks. Cardiac function and morphology were assessed. In this paper was viewed the general characteristics and comorbities associated to obesity. The structure cardiac was determined by weights of the heart and left ventricle (LV). Myocardial function was evaluated by studying isolated papillary muscles from the LV, under the baseline condition and after inotropic and lusitropic maneuvers: myocardial stiffness; postrest contraction; increase in extracellular Ca2+ concentration; change in heart rate and inhibitor of glycolytic pathway. Results: Compared with control group, the obese rats had increased body fat and co-morbities associated with obesity. Functional assessment after blocking iodoacetate shows no difference in the linear regression of DT, however, the RT showed a statistically significant difference in behavior between the control and the obese group, most notable being the slope in group C. Conclusion: The energy imbalance on obesity did not cause cardiac dysfunction. On the contrary, the prioritization of fatty acids utilization provides protection to cardiac muscle during the inhibition of glycolysis, suggesting that this pathway is fewer used by obese cardiac muscle.
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spelling Obesity Preserves Myocardial Function During Blockade of the Glycolytic PathwayA Obesidade Preserva a Função do Miocárdio Durante o Bloqueio da Via GlicolíticaObesidadeRatosMiocárdioMetabolismoÁcidos GraxosObesityRatsMyocardialMetabolismFatty AcidBackground: Obesity is defined by excessive accumulation of body fat relative to lean tissue. Studies during the last few years indicate that cardiac function in obese animals may be preserved, increased or diminished. Objective: Study the energy balance of the myocardium with the hypothesis that the increase in fatty acid oxidation and reduced glucose leads to cardiac dysfunction in obesity. Methods: 30-day-old male Wistar rats were fed standard and hypercaloric diet for 30 weeks. Cardiac function and morphology were assessed. In this paper was viewed the general characteristics and comorbities associated to obesity. The structure cardiac was determined by weights of the heart and left ventricle (LV). Myocardial function was evaluated by studying isolated papillary muscles from the LV, under the baseline condition and after inotropic and lusitropic maneuvers: myocardial stiffness; postrest contraction; increase in extracellular Ca2+ concentration; change in heart rate and inhibitor of glycolytic pathway. Results: Compared with control group, the obese rats had increased body fat and co-morbities associated with obesity. Functional assessment after blocking iodoacetate shows no difference in the linear regression of DT, however, the RT showed a statistically significant difference in behavior between the control and the obese group, most notable being the slope in group C. Conclusion: The energy imbalance on obesity did not cause cardiac dysfunction. On the contrary, the prioritization of fatty acids utilization provides protection to cardiac muscle during the inhibition of glycolysis, suggesting that this pathway is fewer used by obese cardiac muscle.Fundamento: A obesidade é definida por um acúmulo excessivo do tecido adiposo em relação a massa magra tecidual. Estudos realizados nos últimos anos sugerem que a função cardíaca em animais obesos pode se encontrar preservada, aumentada ou reduzida. Objetivo: Estudar o balanço energético do miocárdio com a hipótese de que o aumento na oxidação de ácidos graxos e redução de glicose levam à disfunção cardíaca na obesidade. Métodos: Ratos Wistar machos com 30 dias de idade foram alimentados com uma dieta padrão ou hipercalórica durante 30 semanas. A função e morfologia cardíacas foram analisadas. Neste trabalho foram estudadas as características gerais e comorbidades associadas com a obesidade. A estrutura cardíaca foi determinada pelo peso do coração e do ventrículo esquerdo (VE). A função do miocárdio foi avaliada pela análise de músculos papilares isolados do VE, na condição basal e depois de manobras inotrópicas e lusitrópicas: rigidez do miocárdio, contração pós-pausa, aumento da concentração extracelular de Ca2+, mudança na frequência de estímulos e inibição da via glicolítica. Resultados: Os ratos obesos tiveram um aumento de tecido adiposo e comorbidades associadas à obesidade em relação aos ratos do grupo controle. A análise funcional após o bloqueio pelo iodoacetato não mostrou diferença na regressão linear da tensão desenvolvida (TD), entretanto, a tensão de repouso (TR) apresentou uma diferença estatística significativa entre o grupo controle e o grupo obeso, mais notadamente na inclinação da curva no grupo C. Conclusão: O desequilíbrio energético na obesidade não promoveu disfunção cardíaca. Pelo contrário, a priorização na utilização de ácidos graxos promoveu uma proteção do músculo cardíaco durante a inibição da glicólise, sugerindo que esta via é menos utilizada pelo músculo cardíaco obeso.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Universidade Estadual Paulista Faculdade de Medicina de Botucatu Departamento de Clínica MédicaUniversidade Federal do Espírito Santo Centro de Educação Física e Desportos Departamento de EsportesUniversidade Federal do Mato Grosso Instituto de Ciências da SaúdeUniversidade Federal do Mato Grosso do Sul Escola de FisioterapiaUniversidade Estadual Paulista Instituto de Ciências Biológicas Departamento de BioestatísticaUniversidade Estadual Paulista Faculdade de Medicina de Botucatu Departamento de Clínica MédicaUniversidade Estadual Paulista Instituto de Ciências Biológicas Departamento de BioestatísticaSociedade Brasileira de Cardiologia - SBCUniversidade Estadual Paulista (Unesp)Universidade Federal do Espírito Santo (UFES)Universidade Federal do Mato Grosso Instituto de Ciências da SaúdeUniversidade Federal do Mato Grosso do Sul Escola de FisioterapiaCampos, Dijon Henrique Salomé DeLeopoldo, André SoaresLima-leopoldo, Ana PaulaNascimento, André Ferreira DoOliveira-junior, Silvio Assis DeSilva, Danielle Cristina Tomaz DaSugizaki, Mario MateusPadovani, Carlos Roberto [UNESP]Cicogna, Antonio Carlos [UNESP]2015-02-02T12:39:34Z2015-02-02T12:39:34Z2014-10-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article330-337application/pdfhttp://dx.doi.org/10.5935/abc.20140135Arquivos Brasileiros de Cardiologia. Sociedade Brasileira de Cardiologia - SBC, v. 103, n. 4, p. 330-337, 2014.0066-782Xhttp://hdl.handle.net/11449/11447210.5935/abc.20140135S0066-782X2014002200009S0066-782X2014002200009.pdf94189701035641378727897080522289SciELOreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengArquivos Brasileiros de Cardiologia1.318info:eu-repo/semantics/openAccess2024-08-14T17:21:52Zoai:repositorio.unesp.br:11449/114472Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-14T17:21:52Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway
A Obesidade Preserva a Função do Miocárdio Durante o Bloqueio da Via Glicolítica
title Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway
spellingShingle Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway
Campos, Dijon Henrique Salomé De
Obesidade
Ratos
Miocárdio
Metabolismo
Ácidos Graxos
Obesity
Rats
Myocardial
Metabolism
Fatty Acid
title_short Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway
title_full Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway
title_fullStr Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway
title_full_unstemmed Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway
title_sort Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway
author Campos, Dijon Henrique Salomé De
author_facet Campos, Dijon Henrique Salomé De
Leopoldo, André Soares
Lima-leopoldo, Ana Paula
Nascimento, André Ferreira Do
Oliveira-junior, Silvio Assis De
Silva, Danielle Cristina Tomaz Da
Sugizaki, Mario Mateus
Padovani, Carlos Roberto [UNESP]
Cicogna, Antonio Carlos [UNESP]
author_role author
author2 Leopoldo, André Soares
Lima-leopoldo, Ana Paula
Nascimento, André Ferreira Do
Oliveira-junior, Silvio Assis De
Silva, Danielle Cristina Tomaz Da
Sugizaki, Mario Mateus
Padovani, Carlos Roberto [UNESP]
Cicogna, Antonio Carlos [UNESP]
author2_role author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade Estadual Paulista (Unesp)
Universidade Federal do Espírito Santo (UFES)
Universidade Federal do Mato Grosso Instituto de Ciências da Saúde
Universidade Federal do Mato Grosso do Sul Escola de Fisioterapia
dc.contributor.author.fl_str_mv Campos, Dijon Henrique Salomé De
Leopoldo, André Soares
Lima-leopoldo, Ana Paula
Nascimento, André Ferreira Do
Oliveira-junior, Silvio Assis De
Silva, Danielle Cristina Tomaz Da
Sugizaki, Mario Mateus
Padovani, Carlos Roberto [UNESP]
Cicogna, Antonio Carlos [UNESP]
dc.subject.por.fl_str_mv Obesidade
Ratos
Miocárdio
Metabolismo
Ácidos Graxos
Obesity
Rats
Myocardial
Metabolism
Fatty Acid
topic Obesidade
Ratos
Miocárdio
Metabolismo
Ácidos Graxos
Obesity
Rats
Myocardial
Metabolism
Fatty Acid
description Background: Obesity is defined by excessive accumulation of body fat relative to lean tissue. Studies during the last few years indicate that cardiac function in obese animals may be preserved, increased or diminished. Objective: Study the energy balance of the myocardium with the hypothesis that the increase in fatty acid oxidation and reduced glucose leads to cardiac dysfunction in obesity. Methods: 30-day-old male Wistar rats were fed standard and hypercaloric diet for 30 weeks. Cardiac function and morphology were assessed. In this paper was viewed the general characteristics and comorbities associated to obesity. The structure cardiac was determined by weights of the heart and left ventricle (LV). Myocardial function was evaluated by studying isolated papillary muscles from the LV, under the baseline condition and after inotropic and lusitropic maneuvers: myocardial stiffness; postrest contraction; increase in extracellular Ca2+ concentration; change in heart rate and inhibitor of glycolytic pathway. Results: Compared with control group, the obese rats had increased body fat and co-morbities associated with obesity. Functional assessment after blocking iodoacetate shows no difference in the linear regression of DT, however, the RT showed a statistically significant difference in behavior between the control and the obese group, most notable being the slope in group C. Conclusion: The energy imbalance on obesity did not cause cardiac dysfunction. On the contrary, the prioritization of fatty acids utilization provides protection to cardiac muscle during the inhibition of glycolysis, suggesting that this pathway is fewer used by obese cardiac muscle.
publishDate 2014
dc.date.none.fl_str_mv 2014-10-01
2015-02-02T12:39:34Z
2015-02-02T12:39:34Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.5935/abc.20140135
Arquivos Brasileiros de Cardiologia. Sociedade Brasileira de Cardiologia - SBC, v. 103, n. 4, p. 330-337, 2014.
0066-782X
http://hdl.handle.net/11449/114472
10.5935/abc.20140135
S0066-782X2014002200009
S0066-782X2014002200009.pdf
9418970103564137
8727897080522289
url http://dx.doi.org/10.5935/abc.20140135
http://hdl.handle.net/11449/114472
identifier_str_mv Arquivos Brasileiros de Cardiologia. Sociedade Brasileira de Cardiologia - SBC, v. 103, n. 4, p. 330-337, 2014.
0066-782X
10.5935/abc.20140135
S0066-782X2014002200009
S0066-782X2014002200009.pdf
9418970103564137
8727897080522289
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Arquivos Brasileiros de Cardiologia
1.318
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 330-337
application/pdf
dc.publisher.none.fl_str_mv Sociedade Brasileira de Cardiologia - SBC
publisher.none.fl_str_mv Sociedade Brasileira de Cardiologia - SBC
dc.source.none.fl_str_mv SciELO
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
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