Activated (phosphorylated) JNK is partly responsible for promoting IR in CYP2E1 over-expressed cells [12]. Our results revealed that WT-HFD mice with higher levels of hepatic phospho-JNK developed systemic IR and impaired GT compared to the WT-LFD group (Fig. 4A,C,E). In contrast, no significant differences were observed in JNK phosphorylation, insulin sensitivity, or GT between HFD-fed Cyp2e1-null mice compared to their corresponding LFD-exposed group (Fig. 4B,D,F).
