Palmitate로 유도된 인슐린 저항성 C2C12 근관세포에서 진동 자극에 의한 세포 항상성 회복
Vibration Stimulation Restores Myocellular Homeostasis in Palmitate-Induced Insulin-Resistant C2C12 Myotubes
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Type 2 diabetes is characterized by insulin resistance and mitochondrial dysfunction in skeletal muscle, which is responsible for 80% of postprandial glucose uptake. Vibration is a form of mechanical stimulation that regulates mechanotransduction and activates cellular signaling pathways for skeletal muscle function. We have demonstrated that vibration stimulation improves mitochondrial and metabolic homeostasis in an insulin-resistant C2C12 myotube model. Cells were treated with 0.6 mM palmitate for 24 hours and subjected to vibration at 25 Hz, 0.58 g for 30 minutes per day for 3 days. Cell viability and protein expression of mitochondrial regulators, glucose transporter, myogenic regulatory factor, and apoptotic markers were evaluated using MTT assay and Western blot. Palmitate treatment decreased protein expression of SIRT1, PGC-1, GLUT4, and Myogenin, and increased Bax/Bcl-2 ratio, indicating mitochondrial dysfunction and metabolic impairment. In insulin-resistant myotube, vibration restored mitochondrial biogenesis, glucose uptake, myogenic differentiation, and apoptosis inhibition. In conclusion, vibration activates the SIRT1–PGC-1 pathway, thereby restoring mitochondrial and metabolic homeostasis. Vibration represents a non-invasive mechanical stimulation that has the potential to improve skeletal muscle insulin sensitivity and prevent metabolic muscle disorders.
Abstract
Type 2 diabetes is characterized by insulin resistance and mitochondrial dysfunction in skeletal muscle, which is responsible for 80% of postprandial glucose uptake. Vibration is a form of mechanical stimulation that regulates mechanotransduction and activates cellular signaling pathways for skeletal muscle function. We have demonstrated that vibration stimulation improves mitochondrial and metabolic homeostasis in an insulin-resistant C2C12 myotube model. Cells were treated with 0.6 mM palmitate for 24 hours and subjected to vibration at 25 Hz, 0.58 g for 30 minutes per day for 3 days. Cell viability and protein expression of mitochondrial regulators, glucose transporter, myogenic regulatory factor, and apoptotic markers were evaluated using MTT assay and Western blot. Palmitate treatment decreased protein expression of SIRT1, PGC-1, GLUT4, and Myogenin, and increased Bax/Bcl-2 ratio, indicating mitochondrial dysfunction and metabolic impairment. In insulin-resistant myotube, vibration restored mitochondrial biogenesis, glucose uptake, myogenic differentiation, and apoptosis inhibition. In conclusion, vibration activates the SIRT1–PGC-1 pathway, thereby restoring mitochondrial and metabolic homeostasis. Vibration represents a non-invasive mechanical stimulation that has the potential to improve skeletal muscle insulin sensitivity and prevent metabolic muscle disorders.