Mitigation of chronic glucotoxicity-mediated skeletal muscle atrophy by arachidonic acid

Toxicity caused by chronic hyperglycemia is a significant factor affecting skeletal muscle myogenesis, resulting in diabetic myopathy. Chronic and persistent hyperglycemia causes activation of the atrophy-related pathways in the skeletal muscles, which eventually results in inflammation and muscle degeneration. To counteract this process, various bioactive compound has been studied for their reversal or hypertrophic effect. In this study, we explored the molecular mechanisms associated with reversing glucotoxicity's effect in C2C12 cells by arachidonic acid (AA). We found a substantial increase in the pro-inflammatory cytokines and ROS production in hyperglycemic conditions, mitigated by AA supplementation. We found that AA supplementation restored protein synthesis that was downregulated under glucotoxicity conditions. AA enhanced myogenesis by suppressing high glucose induced inflammation and ROS production and enhancing protein synthesis. These results imply that AA has cytoprotective actions against hyperglycemia-induced cytotoxicity.

Automated summary

This study explored the molecular mechanisms associated with reversing the effects of glucotoxicity on muscle myogenesis through arachidonic acid (AA). The results showed that AA supplementation suppressed inflammation and ROS production induced by high glucose, and enhanced protein synthesis, suggesting its cytoprotective actions against hyperglycemia-induced cytotoxicity.