Carvacrol improves glucose metabolism in type 2 diabetes mellitus by promoting skeletal muscle hypertrophy

Aim To investigate whether carvacrol improves type 2 diabetes(T2D)and modulates skeletal muscle metabolism. Methods A T2D mouse model was established via a combination of streptozotocin (STZ) administration and high-fat diet(HFD) feeding. Carvacrol was administered to evaluate its effects on thermogenesis, gluconeogenesis, and skeletal muscle structural changes. In vivo experiments were performed using HE staining, infrared thermography, and glycogen quantification. In vitro, mouse C2C12 myoblasts were employed to investigate the effects of carvacrol on skeletal muscle hypertrophy and glucose uptake using calcium fluorescence probes, Western blotting, and immunofluorescence. Results Carvacrol promoted extracellular Ca2+ influx into skeletal muscle cells and upregulated the expression of phosphorylated CaMKII, PGC1α, GLUT4, and InsR. These changes enhanced glycogen storage and muscle fiber hypertrophy, thereby increasing glucose uptake capacity in muscle cells. Conclusions Carvacrol activates the classical Ca2+-CaMKII-PGC1α-GLUT4 signaling pathway in skeletal muscle, promoting hypertrophy and metabolic enhancement, and improving glycemic regulation. These findings support the potential of carvacrol as a small-molecule therapeutic agent targeting skeletal muscle in T2D treatment.