In 3T3-L1 cells, celastrol treatment upregulates PGC-1α/glucose transporter type 4 (GLTU4) expression in adipocytes and skeletal muscle via AKT and P38 MAPK, consequently improving insulin resistance, as well as inhibiting gluconeogenic activity through a CREB/PGC-1α pathway [33]. Here, AKT1 is linked to Insulin resistance.