Caracterização de remodelação cardíaca em modelo experimental de obesidade a partir de diferentes tipos de dietas hipercalóricas
Autor(a) principal: | |
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Data de Publicação: | 2017 |
Tipo de documento: | Dissertação |
Idioma: | por |
Título da fonte: | Repositório Institucional da Universidade Federal do Espírito Santo (riUfes) |
Texto Completo: | http://repositorio.ufes.br/handle/10/10513 |
Resumo: | Obesity is a worldwide epidemic and a serious public health problem. Several diseases are associated with excess of adipose tissue, and obesity is considered an independent risk factor for the development of cardiac remodeling and heart failure. The objective of the present study was the development and characterization of an obesity experimental model from hypercaloric diets, a high sucrose (HS), high fat (HF) and high fat and sucrose (HFS), which resulted in cardiac remodeling and predisposition to heart failure. The hypothesis of this investigation was that hypercaloric diets would promote cardiac remodeling, cardiovascular damage and predispose to heart failure, being this condition more evident in the high fat and sucrose model. Wistar rats (n = 60) were randomized into four groups: control (C), high sucrose (HS), high fat (HF) and high fat and sucrose (HFS). General characteristics and comorbidities were measured. The process of cardiac remodeling was evaluated through the weights of the heart, left and right ventricles, atrium, and relationships with the tibia length. The mycoyte cross sectional area and fraction of interstitial collagen of the left ventricle were evaluated. In vivo functional evaluation was determined by hemodynamic and in vitro by analysis of isolated cardiomyocyte. Heart failure was analyzed by pulmonary congestion, right ventricular hypertrophy, and hemodynamic parameters. Data were expressed by mean and standard error of the mean and were submitted to analysis of variance (ANOVA) for independent samples. HF and HFS models led to obesity by increase in adipose tissue deposition and adiposity index (C = 8.3 ± 0.2%, HF = 10.9 ± 0.5%, HFS = 10.2 ± 0.3%, p <0.05). Comorbidities were hypertension, glucose intolerance (HF and HFS) and hyperleptinemia (HF). There was no change in the morphological parameters that characterize the cardiac remodeling process. Regarding the functional analyzes, the obesity promotes reduction in time to 50% of shortening (C = 160 ± 4 ms vs. HF = 134 ± 2, p <0.05) and time to 50% of the relaxation (C: 160 ± 4 ms, HF: 134 ± 3 and HFS: 133 ± 3, p <0.05). The HS model presented contractile dysfunction visualized by reduction in the shortening (C: 8.34 ± 0.32%, HS: 6.91 ± 0.28, p <0.05) and maximal shortening velocity (C: -2, 58 ± 0.10 μm / s, HS: -2.21 ± 0.08, p <0.05). In conclusion, the experimental models proposed in this study were not promote cadiac remodeling and predisposition to heart failure under conditions of obesity or sucrose excess. |
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Leopoldo, Ana Paula LimaLeopoldo, André SoaresMatias, Amanda MartinsSantos, Leonardo dosFerreira, Lucas GuimarãesPadilha, Alessandra SimãoHaraguchi, Fabiano Kenji2018-12-20T13:19:33Z2018-12-202018-12-20T13:19:33Z2017-12-18Obesity is a worldwide epidemic and a serious public health problem. Several diseases are associated with excess of adipose tissue, and obesity is considered an independent risk factor for the development of cardiac remodeling and heart failure. The objective of the present study was the development and characterization of an obesity experimental model from hypercaloric diets, a high sucrose (HS), high fat (HF) and high fat and sucrose (HFS), which resulted in cardiac remodeling and predisposition to heart failure. The hypothesis of this investigation was that hypercaloric diets would promote cardiac remodeling, cardiovascular damage and predispose to heart failure, being this condition more evident in the high fat and sucrose model. Wistar rats (n = 60) were randomized into four groups: control (C), high sucrose (HS), high fat (HF) and high fat and sucrose (HFS). General characteristics and comorbidities were measured. The process of cardiac remodeling was evaluated through the weights of the heart, left and right ventricles, atrium, and relationships with the tibia length. The mycoyte cross sectional area and fraction of interstitial collagen of the left ventricle were evaluated. In vivo functional evaluation was determined by hemodynamic and in vitro by analysis of isolated cardiomyocyte. Heart failure was analyzed by pulmonary congestion, right ventricular hypertrophy, and hemodynamic parameters. Data were expressed by mean and standard error of the mean and were submitted to analysis of variance (ANOVA) for independent samples. HF and HFS models led to obesity by increase in adipose tissue deposition and adiposity index (C = 8.3 ± 0.2%, HF = 10.9 ± 0.5%, HFS = 10.2 ± 0.3%, p <0.05). Comorbidities were hypertension, glucose intolerance (HF and HFS) and hyperleptinemia (HF). There was no change in the morphological parameters that characterize the cardiac remodeling process. Regarding the functional analyzes, the obesity promotes reduction in time to 50% of shortening (C = 160 ± 4 ms vs. HF = 134 ± 2, p <0.05) and time to 50% of the relaxation (C: 160 ± 4 ms, HF: 134 ± 3 and HFS: 133 ± 3, p <0.05). The HS model presented contractile dysfunction visualized by reduction in the shortening (C: 8.34 ± 0.32%, HS: 6.91 ± 0.28, p <0.05) and maximal shortening velocity (C: -2, 58 ± 0.10 μm / s, HS: -2.21 ± 0.08, p <0.05). In conclusion, the experimental models proposed in this study were not promote cadiac remodeling and predisposition to heart failure under conditions of obesity or sucrose excess.A obesidade é considerada uma epidemia mundial e um grave problema de saúde pública. Diversos agravos são associados ao excesso de tecido adiposo, sendo a obesidade considerada fator de risco independente para o desenvolvimento de remodelação e insuficiência cardíaca. O objetivo do presente estudo foi o desenvolvimento e caracterização de um modelo de obesidade experimental a partir de três dietas hipercalóricas, uma hiperglicídica (HG), uma hiperlipídica (HL) e uma hiperlipídica com açúcar (HLA), as quais acarretassem remodelação cardíaca e predisposição à insuficiência cardíaca. A hipótese dessa investigação foi que as dietas hipercalóricas iriam promover remodelação cardíaca, prejuízos cardiovasculares e predispor ao quadro de insuficiência cardíaca, sendo essa condição mais evidente no modelo hiperlipídico com açúcar. Ratos Wistar (n = 60) foram randomizados em quatro grupos: controle (C), hiperglicídico (HG), hiperlipídico (HL) e hiperlipídica com açúcar (HLA). Foram mensurados características gerais e comorbidades. O processo de remodelação cardíaca foi avaliado por meio dos pesos do coração, câmaras cardíacas e relações com o comprimento da tíbia, bem como, microscópicamente, a partir da determinação da área seccional transversa do miócito e fração de colágeno intersticial do ventrículo esquerdo (VE). A avaliação funcional in vivo foi determinada pela análise hemodinâmica e in vitro por meio da técnica de cardiomiócito isolado. A insuficiência cardíaca foi analisada pela congestão pulmonar, hipertrofia do ventrículo direito (VD), e parâmetros hemodinâmicos. Os dados foram expressos por média e erro padrão da média, sendo submetidos à análise de variância (ANOVA) para amostras independentes. O nível de significância considerado foi de 5%. Os resultados demonstram que os modelos HL e HLA acarretaram obesidade a partir do aumento dos depósitos de tecido adiposo e índice de adiposidade (C= 8,3 ± 0,2%; HL= 10,9 ± 0,5%; HLA= 10,2 ± 0,3%; p<0,05). As comorbidades encontradas foram hipertensão arterial, intolerância à glicose (HL e HLA) e hiperleptinemia (HL). Não houve alteração nos parâmetros morfológicos que caracterizassem o processo de remodelação cardíaca. Em relação às análises funcionais, a obesidade promoveu melhora pontual, observadas por redução no tempo até 50% do encurtamento (C= 160 ± 4 ms vs. HL= 134 ± 2, p< 0,05) e tempo até 50% do relaxamento (C: 160 ± 4 ms; HL: 134 ± 3 e HLA: 133 ± 3, p< 0,05). O modelo HG acarretou disfunção contrátil leve visualizada por menor percentual (C: 8,34 ± 0,32%; HG: 6,91 ± 0,28; p<0,05) e velocidade máxima de encurtamento (C: -2,58 ± 0,10 µm/s; HG: -2,21 ± 0,08; p< 0,05). Em conclusão, os modelos experimentais proposto neste estudo não foram capazes de promover remodelação e predisposição à insuficiência cardíaca sob condições de obesidade ou excesso de sacarose.Texthttp://repositorio.ufes.br/handle/10/10513porUniversidade Federal do Espírito SantoMestrado em Nutrição e SaúdePrograma de Pós-Graduação em Nutrição e SaúdeUFESBRCentro de Ciências da SaúdeObesityHypercaloric dietsMyocardial remodelingHeart failureObesidadeDietas hipercalóricasRemodelação miocárdicaInsuficiência cardíacaNutriçãoCaracterização de remodelação cardíaca em modelo experimental de obesidade a partir de diferentes tipos de dietas hipercalóricasinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)instname:Universidade Federal do Espírito Santo (UFES)instacron:UFESORIGINALtese_11690_Dissertação Amanda Matias - Versão PDF - PPGNS.pdfapplication/pdf2279983http://repositorio.ufes.br/bitstreams/563374fa-e66d-4640-87b4-3e6566c619c6/download52bb1cf857bae61a2ec42519e94fdd1eMD5110/105132024-07-16 17:05:39.21oai:repositorio.ufes.br:10/10513http://repositorio.ufes.brRepositório InstitucionalPUBhttp://repositorio.ufes.br/oai/requestopendoar:21082024-10-15T17:51:07.689743Repositório Institucional da Universidade Federal do Espírito Santo (riUfes) - Universidade Federal do Espírito Santo (UFES)false |
dc.title.none.fl_str_mv |
Caracterização de remodelação cardíaca em modelo experimental de obesidade a partir de diferentes tipos de dietas hipercalóricas |
title |
Caracterização de remodelação cardíaca em modelo experimental de obesidade a partir de diferentes tipos de dietas hipercalóricas |
spellingShingle |
Caracterização de remodelação cardíaca em modelo experimental de obesidade a partir de diferentes tipos de dietas hipercalóricas Matias, Amanda Martins Obesity Hypercaloric diets Myocardial remodeling Heart failure Obesidade Dietas hipercalóricas Remodelação miocárdica Insuficiência cardíaca Nutrição |
title_short |
Caracterização de remodelação cardíaca em modelo experimental de obesidade a partir de diferentes tipos de dietas hipercalóricas |
title_full |
Caracterização de remodelação cardíaca em modelo experimental de obesidade a partir de diferentes tipos de dietas hipercalóricas |
title_fullStr |
Caracterização de remodelação cardíaca em modelo experimental de obesidade a partir de diferentes tipos de dietas hipercalóricas |
title_full_unstemmed |
Caracterização de remodelação cardíaca em modelo experimental de obesidade a partir de diferentes tipos de dietas hipercalóricas |
title_sort |
Caracterização de remodelação cardíaca em modelo experimental de obesidade a partir de diferentes tipos de dietas hipercalóricas |
author |
Matias, Amanda Martins |
author_facet |
Matias, Amanda Martins |
author_role |
author |
dc.contributor.advisor-co1.fl_str_mv |
Leopoldo, Ana Paula Lima |
dc.contributor.advisor1.fl_str_mv |
Leopoldo, André Soares |
dc.contributor.author.fl_str_mv |
Matias, Amanda Martins |
dc.contributor.referee1.fl_str_mv |
Santos, Leonardo dos |
dc.contributor.referee2.fl_str_mv |
Ferreira, Lucas Guimarães |
dc.contributor.referee3.fl_str_mv |
Padilha, Alessandra Simão |
dc.contributor.referee4.fl_str_mv |
Haraguchi, Fabiano Kenji |
contributor_str_mv |
Leopoldo, Ana Paula Lima Leopoldo, André Soares Santos, Leonardo dos Ferreira, Lucas Guimarães Padilha, Alessandra Simão Haraguchi, Fabiano Kenji |
dc.subject.eng.fl_str_mv |
Obesity Hypercaloric diets Myocardial remodeling Heart failure |
topic |
Obesity Hypercaloric diets Myocardial remodeling Heart failure Obesidade Dietas hipercalóricas Remodelação miocárdica Insuficiência cardíaca Nutrição |
dc.subject.por.fl_str_mv |
Obesidade Dietas hipercalóricas Remodelação miocárdica Insuficiência cardíaca |
dc.subject.cnpq.fl_str_mv |
Nutrição |
description |
Obesity is a worldwide epidemic and a serious public health problem. Several diseases are associated with excess of adipose tissue, and obesity is considered an independent risk factor for the development of cardiac remodeling and heart failure. The objective of the present study was the development and characterization of an obesity experimental model from hypercaloric diets, a high sucrose (HS), high fat (HF) and high fat and sucrose (HFS), which resulted in cardiac remodeling and predisposition to heart failure. The hypothesis of this investigation was that hypercaloric diets would promote cardiac remodeling, cardiovascular damage and predispose to heart failure, being this condition more evident in the high fat and sucrose model. Wistar rats (n = 60) were randomized into four groups: control (C), high sucrose (HS), high fat (HF) and high fat and sucrose (HFS). General characteristics and comorbidities were measured. The process of cardiac remodeling was evaluated through the weights of the heart, left and right ventricles, atrium, and relationships with the tibia length. The mycoyte cross sectional area and fraction of interstitial collagen of the left ventricle were evaluated. In vivo functional evaluation was determined by hemodynamic and in vitro by analysis of isolated cardiomyocyte. Heart failure was analyzed by pulmonary congestion, right ventricular hypertrophy, and hemodynamic parameters. Data were expressed by mean and standard error of the mean and were submitted to analysis of variance (ANOVA) for independent samples. HF and HFS models led to obesity by increase in adipose tissue deposition and adiposity index (C = 8.3 ± 0.2%, HF = 10.9 ± 0.5%, HFS = 10.2 ± 0.3%, p <0.05). Comorbidities were hypertension, glucose intolerance (HF and HFS) and hyperleptinemia (HF). There was no change in the morphological parameters that characterize the cardiac remodeling process. Regarding the functional analyzes, the obesity promotes reduction in time to 50% of shortening (C = 160 ± 4 ms vs. HF = 134 ± 2, p <0.05) and time to 50% of the relaxation (C: 160 ± 4 ms, HF: 134 ± 3 and HFS: 133 ± 3, p <0.05). The HS model presented contractile dysfunction visualized by reduction in the shortening (C: 8.34 ± 0.32%, HS: 6.91 ± 0.28, p <0.05) and maximal shortening velocity (C: -2, 58 ± 0.10 μm / s, HS: -2.21 ± 0.08, p <0.05). In conclusion, the experimental models proposed in this study were not promote cadiac remodeling and predisposition to heart failure under conditions of obesity or sucrose excess. |
publishDate |
2017 |
dc.date.issued.fl_str_mv |
2017-12-18 |
dc.date.accessioned.fl_str_mv |
2018-12-20T13:19:33Z |
dc.date.available.fl_str_mv |
2018-12-20 2018-12-20T13:19:33Z |
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info:eu-repo/semantics/publishedVersion |
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info:eu-repo/semantics/masterThesis |
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masterThesis |
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publishedVersion |
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http://repositorio.ufes.br/handle/10/10513 |
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http://repositorio.ufes.br/handle/10/10513 |
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por |
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info:eu-repo/semantics/openAccess |
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openAccess |
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Text |
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Universidade Federal do Espírito Santo Mestrado em Nutrição e Saúde |
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Programa de Pós-Graduação em Nutrição e Saúde |
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UFES |
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BR |
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Centro de Ciências da Saúde |
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Universidade Federal do Espírito Santo Mestrado em Nutrição e Saúde |
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reponame:Repositório Institucional da Universidade Federal do Espírito Santo (riUfes) instname:Universidade Federal do Espírito Santo (UFES) instacron:UFES |
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Repositório Institucional da Universidade Federal do Espírito Santo (riUfes) |
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