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Doctoral Thesis
DOI
Document
Author
Full name
Marco Aurelio Salomão Fortes
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2018
Supervisor
Committee
Curi, Rui (President)
Bazotte, Roberto Barbosa
Boaventura, Maria Fernanda Cury
Rosa Neto, José Cesar
Silva, Aline David
Title in Portuguese
Hipertrofia dos músculos sóleo e EDL de ratos no início do diabetes induzido por estreptozotocina.
Keywords in Portuguese
Músculo esquelético; Síntese de Proteínas; Força muscular; Hiperglicemia; Eletroestimulação;
Abstract in Portuguese
Pacientes com diabetes mellitus apresentam perda de massa e força muscular esquelética. O treinamento de força é prescrito aos pacientes diabéticos como parte do tratamento, pois melhora o controle glicêmico além de promover aumento da massa muscular. Foram investigados os mecanismos envolvidos na hipertrofia muscular induzida por sobrecarga mecânica durante o estabelecimento do estado diabético do tipo I induzido por estreptozotocina em ratos. Os experimentos foram realizados nos músculos com predominância de fibras oxidativas (sóleo) ou glicolíticas (extensor digital longo - EDL). Avaliou-se a modulação da via de síntese de proteínas PI3K-AKT-mTOR sete dias após indução de hipertrofia dos músculos sóleo por tenotomia do músculo gastrocnêmio e do EDL pela ablação do músculo tibial. Determinou-se também a expressão de mRNA de outras vias de sinalização que controlam a hipertrofia muscular: mecanotransdução (FAK), Wnt/β-catenina e miostatina e folistatina. Os músculos sóleo e EDL quando submetidos à sobrecarga funcional sofreram hipertrofia semelhante em animais controles e diabéticos. O aumento das forças tetânica e isotônica, absolutas e específicas, ocorreu na mesma magnitude que a hipertrofia muscular. A hipertrofia do músculo EDL nos animais diabéticos envolveu principalmente a via PI3K-AKT-mTOR além da redução no conteúdo de AMPK e diminuição da expressão de miostatina. No músculo sóleo, a hipertrofia foi mais pronunciada nos animais diabéticos por ativação mais intensa da via pelas proteínas rpS6 e aumento na expressão de mRNA de IGF-1, MGF e folistatina além de diminuição nos conteúdos de miostatina, MuRF-1 e atrogina-1. As modificações relacionadas à sinalização permitiram ao músculo sóleo alcançar valores de força e massa muscular similares ao grupo controle.
Title in English
Hypertrophy of soleus and EDL muscles in the early diabetes induced by streptozotocin in rats.
Keywords in English
Skeletal muscle; protein synthesis; muscle strength; hyperglycemia; electrostimulation
Abstract in English
Patients with diabetes mellitus have reduction in skeletal muscle mass and strength. Strength training is prescribed to diabetic patients as part of the treatment since it improves glycemic control and promotes an increase of skeletal muscle mass. The mechanisms involved in the overload-induced muscle hypertrophy during the establishment of the type I diabetic state, induced by streptozotocin, were investigated in rats. The experiments were performed in muscles with predominance of oxidative (soleus) or glycolytic (EDL) fibers. PI3K/AKT/mTOR protein synthesis pathway was evaluated seven days after the overload-induced hypertrophy of the soleus muscle by tenotomy of the gastrocnemius muscle and of the EDL muscle by tibialis anterior muscle ablation. The mRNA expression of genes associated with different signaling pathways that control muscle hypertrophy was also evaluated: mechanotransduction (FAK) signaling, Wnt/β-catenin, myostatin and follistatin. The soleus and EDL muscles when submitted to overload had similar hypertrophic responses in control and diabetic animals. The increase of twitch and tetanic, absolute and specific, forces had the same magnitude as the muscle hypertrophic response. Hypertrophy of the EDL muscle from diabetic animals mostly involved mechanical loading-stimulated PI3K/AKT/mTOR pathway in addition to the reduced activation of AMPK and decrease of myostatin expression. Hypertrophy was more pronounced in the soleus muscle of diabetic animals due to a more potent activation of rpS6 and increased mRNA expression of IGF-1, MGF and follistatin, and decrease of the myostatin, MuRF-1 and atrogin-1 contents. The activated signaling pathways enabled the soleus muscle mass and force of the diabetic rats to reach the values of the control group.
 
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Publishing Date
2019-05-08
 
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