Silencing miR-106b improves palmitic acid-induced mitochondrial dysfunction and insulin resistance in skeletal myocytes.
Mol Med Rep
; 11(5): 3834-41, 2015 May.
Article
en En
| MEDLINE
| ID: mdl-25529328
ABSTRACT
MicroRNA106b (miR106b) is reported to correlate closely with skeletal muscle insulin resistance. In the current study the effect of miR106b on palmitic acid (PA)induced mitochondrial dysfunction and insulin resistance was investigated in C2C12 myotubes via the silencing of miR106b. MiR106b expression was increased under PA treatment, while miR106b loss of function improved insulin sensitivity by upregulating its target mitofusin2 (Mfn2) in C2C12 myocytes. Furthermore, miR106b loss of function partly improved mitochondrial morphological lesions and increased the levels of mitochondial DNA and intracellular adenosine triphosphate that had been impaired by PA exposure in C2C12 myocytes. MiR106b loss of function attenuated the levels of intracellular reactive oxygen species (ROS), and upregulated the expression levels of the estrogenrelated receptor (ERR)α/peroxisome proliferative activated receptor γ coactivator (PGC)1α/Mfn2 axis under PA exposure. In addition, miR106b negatively regulated skeletal muscle mitochondrial function and insulin sensitivity under PAinduced insulin resistance by targeting Mfn2, which may be associated with reduced ROS and upregulation of the ERRα/PGC1α/Mfn2 axis.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Resistencia a la Insulina
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Fibras Musculares Esqueléticas
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Ácido Palmítico
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Silenciador del Gen
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MicroARNs
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Mitocondrias
Límite:
Animals
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Humans
Idioma:
En
Revista:
Mol Med Rep
Año:
2015
Tipo del documento:
Article