PPARG and Insulin resistance: Chronic treatment of rodent pre-adipocytes, 3T3-F442A and 3T3-L1, with IL-6 increased their autocrine IL-6 secretion and promoted insulin resistance consistent with downregulation of Glut4 in adipocytes and other pro-adipogenic nuclear factors such as peroxisome proliferator-activated receptor γ (Pparγ, also known as PPARG) and CCAAT/enhancer-binding protein α (Cebpα; also known as CEBPA) [26].