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.

Author(s)

Flávia de Toledo Frias

• Document type: Master's Dissertation
• Press: São Paulo.
• Institution: Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI)
• Defense date: 2016-05-13

Examining board members

Alice Cristina Rodrigues; William Tadeu Lara Festuccia; Edilamar Menezes de Oliveira

• Advisor: Alice Cristina Rodrigues

Abstract

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. (AU)

• FAPESP's process: 13/19787-0 - The role of microRNAs (miR-1, miR-133, miR-206, miR-208b, miR-499 e miR-223)in skeletal muscle of C57BL/6 mouse during insulin resistance
• Grantee: Flávia de Toledo Frias
• Support Opportunities: Scholarships in Brazil - Master