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Master's Dissertation
DOI
10.11606/D.42.2016.tde-12092016-085246
Document
Author
Full name
Flávia de Toledo Frias
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2016
Supervisor
Committee
Rodrigues, Alice Cristina (President)
Festuccia, William Tadeu Lara
Oliveira, Edilamar Menezes de
Title in Portuguese
Papel dos microRNAs (miR-1, miR-133, miR-206, miR-208b, miR-499 e miR-223) no músculo esquelético de camundongos C57BL/6 durante o estado de resistência à insulina.
Keywords in Portuguese
Metabolismo muscular
MicroRNAs
Mitocôndria
Resistência à insulina
Abstract in Portuguese
No músculo esquelético (ME) resistente à insulina, a disponibilidade elevada de ácidos graxos (AGs) livres observada na obesidade provoca alterações na função mitocondrial. Sendo os microRNAs (miRs) moléculas recentemente apontadas na regulação gênica de vias metabólicas, nosso objetivo foi investigar em ME de camundongos com resistência à insulina (RI) induzida por dieta hiperlipídica durante 8 semanas, tratados com fenofibrato (CF e HF) ou metilcelulose (veículo; grupos C e H) nas duas semanas antes do sacrifício, se os miRs-1a, 133a/b, 206, 208b, 499 e miR-223 participam da patogênese da RI. O quadro de RI foi induzido no grupo H e o fenofibrato reverteu parcialmente a RI (grupo HF) observada através das alterações em parâmetros metabólicos e enzimáticos, que parecem ser mediados pelo miR-1a regulando a proteína AMPKα2. O aumento na transcrição de AMPKα2 ativa processos catabólicos tais como a captação de glicose e oxidação de AGs, sendo considerada a principal enzima reguladora do metabolismo celular ao estimular a expressão de genes mitocondriais via PGC-1α.
Title in English
MicroRNAs role (miR-1, miR-133, miR-206, miR-208b, miR-499 e miR-223) in skeletal muscle of C57BL/6 mice during insulin resistance state.
Keywords in English
Insulin resistance
MicroRNAs
Mitochondria
Skeletal muscle metabolism
Abstract in English
In skeletal muscle (SM) tissue, evidences suggest that the high availability of free fatty acids (FFAs) observed in obesity plays a central role in the development of insulin resistance (IR) by causing changes in mitochondrial function. Since microRNAs (miRs) are recently identified molecules acting as gene regulators of metabolic pathways, we aimed to investigate in SM of insulin resistant mice induced by 8 weeks of high-fat diet (HFD) feeding, treated with fenofibrate (CF and HF) or metilcelulose (vehicle, C and H) two weeks before euthanasia, if miRs-1a, 133a/b, 206, 208b, 499 and 223 are involved in IR pathogenesis. IR was induced after 8 weeks of HFD (H), and fenofibrate treatment (HF) partially reverted this condition by causing alterations on metabolic and enzymatic parameters, which seems to be mediated by miR-1a regulating AMPKα2 protein. AMPKα2 increased translation active catabolic processes such as glucose uptake and FFAs oxidation, being considered the main regulator of cell metabolism by stimulating mitochondrial genes expression via PGC-1α.
 
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Release Date
2018-09-12
Publishing Date
2016-09-12
 
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