Author(s): LI, H.H., WU, Z.J., LIN, T.Y., HUNG, W., Institution: NATIONAL TAIWAN UNIVERSITY OF SPORT, Country: TAIWAN, Abstract-ID: 1689

INTRODUCTION:
The prevalence of obesity and its associated complications, such as type 2 diabetes and cardiovascular disease, has significantly increased. Reactive oxygen species (ROS) and insulin resistance are well-known for their key roles in the development of these diseases, particularly in skeletal muscle. Regular exercise has emerged as one of the most effective therapeutic strategies for preventing and treating these conditions. Additionally, evidence supports the notion that ROS including exercise and muscle contraction, which are a necessary component for glucose cell transport and adaptation to physiological stress. Numerous studies have confirmed that exercise plays a crucial role in improving insulin signaling and attenuating oxidative stress, primarily in mitigating the impact of these diseases. However, the detailed molecular mechanisms underlying the effect of exercise on lipotoxicity-induced muscle damage such as insulin resistance and oxidative stress in muscle remain largely unclear. Electrical pulse stimulation (EPS) has been employed as an in vitro exercise model in skeletal muscle cells. This study aims to investigate the effects of EPS stimulation in attenuating free fatty acids (FFAs)-induced myotube lipotoxicity, which includes insulin resistance and oxidative stress.
METHODS:
Mouse C2C12 myoblasts were differentiated into C2C12 myotubes. The myotubes were incubated with palmitic acid for 24 hours followed by treatment with electrical pulse stimulation (EPS) for 3 hours. The expression of myokines, notably interleukin-6 (IL-6), was evaluated using both RT-PCR and enzyme-linked immunosorbent assay (ELISA). Insulin resistance markers, such as pIRS-1 and pAkt protein expressions, were assessed via western blotting. Oxidative stress levels were determined using 2-7dichlorofluorescin diacetate (DCFH-DA) staining. Furthermore, the expression of antioxidants, including SOD1, SOD2, and HO-1, was analyzed using RT-PCR and western blotting.
RESULTS:
The EPS stimulation resulted in increased expression of myokines, including IL-6, in C2C12 myotubes. Additionally, EPS stimulation attenuated FFAs-induced insulin resistance. Moreover, the expression of antioxidants, including SOD1, SOD2, and HO-1, was higher in EPS-treated myotubes compared to those exposed to FFAs-induced lipotoxicity in C2C12 cells.
CONCLUSION:
The electrical pulse stimulation (EPS) was found to mitigate free fatty acid (FFA)-induced muscle damage in C2C12 myotubes, including the alleviation of insulin resistance and oxidative stress.