Transition from physical activity to inactivity increases skeletal muscle miR-148b content and triggers insulin resistance.
Caroline GasteboisStéphanie ChanonSophie RomeChristine DurandElise PelasciniAudrey JalabertVanessa EuthineVincent PialouxStéphane BlancChantal SimonEtienne LefaiPublished in: Physiological reports (2017)
This study investigated miR-148b as a potential physiological actor of physical inactivity-induced effects in skeletal muscle. By using animal and human protocols, we demonstrated that the early phase of transition toward inactivity was associated with an increase in muscle miR-148b content, which triggered the downregulation of NRAS and ROCK1 target genes. Using human myotubes, we demonstrated that overexpression of miR-148b decreased NRAS and ROCK1 protein levels, and PKB phosphorylation and glucose uptake in response to insulin. Increase in muscle miR-148b content might thus participate in the decrease in insulin sensitivity at the whole body level during the transition toward physical inactivity.
Keyphrases
- skeletal muscle
- insulin resistance
- physical activity
- endothelial cells
- type diabetes
- cell proliferation
- mental health
- high glucose
- pluripotent stem cells
- high fat diet
- induced pluripotent stem cells
- polycystic ovary syndrome
- transcription factor
- signaling pathway
- gene expression
- glycemic control
- wild type
- oxidative stress
- body mass index
- risk assessment
- dna methylation
- blood glucose
- small molecule
- binding protein
- high resolution
- climate change
- genome wide identification