FER1L6 ameliorates insulin resistance by regulating GLUT4 expression

Insulin resistance, a prominent characteristic of type 2 diabetes, has been extensively studied. In our investigation, we examined the effect of Eudesmin on insulin resistance in 3T3-L1 adipocytes and HepG2 cells. Additionally, we analyzed the alterations in mRNA expression in insulin-resistant HepG2 cells through transcriptomic techniques. Subsequently, we assessed the changes in mRNA expression in insulin-resistant HepG2 cells following Eudesmin treatment. Our analysis revealed 13 differentially expressed genes that were commonly observed. Notably, FER1L6 exhibited the most significant changes, with a marked upregulation in mRNA expression in insulin-resistant HepG2 cells. Consequently, we conducted functional experiments to validate the role of fer-1 like family member 6 (FER1L6). Specifically, through gene knockdown experiments, we observed a significant enhancement in glucose transporter type 4 (GLUT4) expression and an improvement in insulin resistance status in cell models. Therefore, FER1L6 emerges as a promising therapeutic target for insulin resistance.