Sodium benzoate, a common food preservative-induced Insulin resistance and atrophy in C2C12 myotubes.

Sodium benzoate (SB), a widely used food preservative, has been reported to possess several therapeutic benefits including treating neurodegenerative disorders as well as negative effects such as altering glucose homeostasis. However, limited attention has been given to its role in inducing insulin resistance (IR). Therefore, current study was designed to investigate the relationship between SB and insulin resistance using C2C12 myotubes and to explore the possible underlying mechanisms. Myotubes were exposed to SB (20 mM) for 24 h and glucose consumption and uptake assays along with confocal microscopy (GLUT4 translocation) were used to evaluate IR. Oxidative stress indicators i.e. reactive oxygen species (ROS), lipid peroxidation (LPO), and reduced glutathione (GSH) levels were also measured. Myotubes morphology along with atrophic markers (calpain activity) were evaluated. Data show that in C2C12 myotubes, SB treatment reduced glucose consumption and uptake in a dose-dependent manner. SB inducing IR by disrupting insulin-mediated GLUT4 translocation in cultured myotubes. Alteration in oxidative stress-related markers (i.e. elevated ROS and LPO levels, reduced GSH) were also observed in SB-treated myotubes. Furthermore, decrease in the fusion index, length, and diameter of myotubes along with upregulation of calpain activity and decrease in muscle protein were also observed. Study concludes that SB exposure not only induced IR but also caused atrophy and oxidative stress in the C2C12 myotubes.