Endoplasmic reticulum (ER) stress aggravates diaphragm weakness through activating PERK/JNK signaling in obesity hypoventilation syndrome
Authors' conclusion
These data suggest that ectopic lipid deposition impairs the diaphragmatic function of people with obesity. Activation of PERK/JNK signaling is involved in the pathogenesis of lipotoxicity-induced diaphragm weakness in obesity hypoventilation syndrome.
Study context
- Population
- People with obesity (obesity hypoventilation syndrome context); mice fed a high-fat diet for 24 weeks; C2C12 myotubes
- Comparison
- People with obesity vs controls; high-fat diet obese mice; PERK or JNK inhibition in C2C12 myotubes
- Outcome
- Diaphragmatic function, lipid deposition and ER stress signaling
Methodological detailshuman patients, obese mice and C2C12 myotubes
- Human patients, obese mice and C2C12 myotubes
Main finding
As reported in the abstract
- People with obesity showed significant diaphragm weakness and lipid accumulation, confirmed in obese mice
- Diaphragms of obese mice: altered lipid-metabolism gene expression and ER stress activation (elevated PERK and JNK activation)
- In C2C12 myotubes, PERK or JNK inhibition abrogated lipotoxicity-induced intracellular lipid deposition and insulin resistance
- JNK inhibition reversed lipotoxicity-induced impairment of elasticity in C2C12 myotubes
Original publication
ER stress aggravates diaphragm weakness through activating PERK/JNK signaling in obesity hypoventilation syndrome. Obesity (Silver Spring). Published 21 July 2023. doi:10.
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