This may be because FGF21 increased the phosphorylation of insulin signaling-related proteins (e.g., insulin receptor substrate 1 (IRS1) and Akt), inhibited the activation of NF-κB inflammatory factors, promoted glycogen conversion (e.g., glucose transporter type 1 (GLUT1) and GLUT4), and elevated the expression of β-Klotho in the skeletal muscle myotube insulin-resistance model constructed by exogenous drugs [105]. Here, INS is linked to Insulin resistance.