Efeito do treinamento resistido sobre a expressão de genes mitocondriais, parâmetros cardiovasculares, hepáticos e séricos de animais obesos induzidos por dieta hipercalórica
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Data
2018-05-18
Autores
Laurindo, Caroline Pancera
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Universidade Estadual Paulista (Unesp)
Resumo
Introdução: A obesidade está ligada a progressão de doenças crônicas associadas à disfunção mitocondrial. O treinamento de resistência pode ser considerado uma abordagem válida para reversão desses fatores ainda pouco explorados na população obesa. Objetivo: Investigar o efeito do treinamento resistido sobre a composição corporal, colesterol e glicose circulantes, alterações cardiovasculares e hepáticas e sobre a expressão de genes do metabolismo mitocondrial de ratos obesos induzidos por dieta hipercalórica. Métodos: Foram utilizados 36 ratos machos Wistar, aleatoriamente separados em Controle Sedentário (CS), Controle Exercitado (CE), Obeso Sedentário (OS) e Obeso Exercitado (OE). Para os animais obesos foi ofertada uma dieta hipercalórica (D.H). O treinamento resistido (T.R) foi progressivo durante 12 semanas com base na Repetição Máxima (RM), com carga a partir de 50% até 100% PC. Os tecidos, coração, pulmão e fígado foram coletados para análise histológica, sangue para análises séricas, músculo esquelético gastrocnêmio para análise da expressão de genes pela técnica de RT-PCR e tecido adiposo para mensuração da adiposidade. Foram utilizados os testes de Anova- One Way e Kruskall Wallis. Resultados: O Grupo OS se destacou pela quantidade de triglicerídeos (p<0,0001) e glicose circulantes (p<0,001). Foi detectado aumento na espessura da artéria pulmonar e ventrículo direito (VD) no grupo OS (p<0,0001). Na análise Fractal o VD apresentou diferença entre OS e CE (p=0,04). Na análise de hepática, o grupo OS apresentava uma quantidade de macrófagos acima da encontrada para os demais grupos (p<0,0001), além do triplo de quadros de esteatose (p=0,0002). A expressão de Ppargc1a (PGC1-α) foi 4x maior no grupo CE do que no grupo OS, e 3x maior no grupo OE (p=0,007) comparado ao OS. No grupo OS houve diminuição de Mfn2 (p=0,02), aumento de Fis1 (p=0,006), redução em ~65% na expressão de Nos3 (p=0,02), e acréscimo de 60% na expressão de MnSod (p=0,008) em comparação a OE. Conclusão: A prática de exercício resistido foi eficaz em amenizar o desenvolvimento da obesidade e suas comorbidades como dislipidemia, esteatose hepática e complicações cardiovasculares, além de manter e melhorar a expressão de genes mitocondriais.
Introduction: Obesity is linked to the progression of chronic diseases associated to mitochondrial dysfunction. Resistance training can be considered a valid approach to reverse these factors that are still poorly explored in obese. Objective: To address the effect of resistive training on body composition, circulating cholesterol and glucose, cardiovascular and hepatic alterations, and on mitochondrial gene expression. Noting the role of resistance training in preventing, maintaining or increasing these factors. Methods: Thirty - six male Wistar rats were divided in Control Sedentary (CS), Control Exercised (CE), Obese Sedentary (OS) and Obese Exercised (OE) groups. Obese animals were offered a hypercaloric diet (HD). Resistance training (RT) was progressive for 12 weeks based on Maximum Repetition (MR), with load from 50% to 100% of BW. The tissues, heart, lung and liver were collected for histological analysis, blood for serum analysis, gastrocnemius skeletal muscle for analysis of gene expression by the RT-PCR and periepidydimal adipose tissue was removed to measure adiposity level. Anova-One Way and Kruskall Wallis tests were used. Results: OS group was distinguished by the amount of circulating triglycerides (p <0.0001) and glucose (p <0.001). Increased thickness of the pulmonary artery and right ventricle (RV) in the OS group was detected (p <0.0001). In the Fractal analysis the RV presented difference between OS and CE (p = 0.04). In hepatic analysis, the OS group had a higher amount of macrophages than the other groups (p <0.0001), in addition to triple steatosis (p = 0.0002). The expression of Ppargc1a (PGC1-α) was 4x higher in the CE group than in the OS group, and 3x higher in the OE group (p = 0.007) compared to OS. There was decreased Mfn2 (p = 0.02), increased Fis1 (p = 0.006), reduced (~ 65%) Nos3 (p = 0.02), and 60%-increased MnSod genes expression (p = 0.008) compared to OE. Conclusion: Regular resistive training was effective in softening the development of obesity and its comorbidities, such as dyslipidemia, hepatic steatosis and cardiovascular complications, in addition to maintaining and improving the expression of mitochondrial genes.
Introduction: Obesity is linked to the progression of chronic diseases associated to mitochondrial dysfunction. Resistance training can be considered a valid approach to reverse these factors that are still poorly explored in obese. Objective: To address the effect of resistive training on body composition, circulating cholesterol and glucose, cardiovascular and hepatic alterations, and on mitochondrial gene expression. Noting the role of resistance training in preventing, maintaining or increasing these factors. Methods: Thirty - six male Wistar rats were divided in Control Sedentary (CS), Control Exercised (CE), Obese Sedentary (OS) and Obese Exercised (OE) groups. Obese animals were offered a hypercaloric diet (HD). Resistance training (RT) was progressive for 12 weeks based on Maximum Repetition (MR), with load from 50% to 100% of BW. The tissues, heart, lung and liver were collected for histological analysis, blood for serum analysis, gastrocnemius skeletal muscle for analysis of gene expression by the RT-PCR and periepidydimal adipose tissue was removed to measure adiposity level. Anova-One Way and Kruskall Wallis tests were used. Results: OS group was distinguished by the amount of circulating triglycerides (p <0.0001) and glucose (p <0.001). Increased thickness of the pulmonary artery and right ventricle (RV) in the OS group was detected (p <0.0001). In the Fractal analysis the RV presented difference between OS and CE (p = 0.04). In hepatic analysis, the OS group had a higher amount of macrophages than the other groups (p <0.0001), in addition to triple steatosis (p = 0.0002). The expression of Ppargc1a (PGC1-α) was 4x higher in the CE group than in the OS group, and 3x higher in the OE group (p = 0.007) compared to OS. There was decreased Mfn2 (p = 0.02), increased Fis1 (p = 0.006), reduced (~ 65%) Nos3 (p = 0.02), and 60%-increased MnSod genes expression (p = 0.008) compared to OE. Conclusion: Regular resistive training was effective in softening the development of obesity and its comorbidities, such as dyslipidemia, hepatic steatosis and cardiovascular complications, in addition to maintaining and improving the expression of mitochondrial genes.
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Palavras-chave
Obesidade, Treinamento resistido, Mitocôndrias, Obesity, Resistance training, Mitochondria