【Objective】 To investigate the effect of interleukin-17A on insulin resistance in hepatocyte steatosis model cells. 【Methods】 The model of hepatocyte steatosis in HepG2 cells was generated by oleic-acid and then cells were treated with or without interleukin-17A to classify its role in insulin signaling pathway. 【Results】No significant change was observed in p-AKT

p-PI3K phosphorylation levels in HepG2 cells treated with IL–17A alone

so as the glucose uptake

glycogen synthesis of p-GSK3β

gluconeogenesis of p-FOXO1/G-6-pase/PEPCK or p-JNK/p-c-jun in the JNK pathway. However

in high-fat induced fatty degeneration HepG2 cells model

intervention with interleukin-17A further induced insulin resistance effect

sharply inhibited cell insulin signaling molecules

and significantly decreased p-AKT

p-PI3K phosphorylation levels

resulting in decreased glucose intake

glycogen synthesis

and increased gluconeogenesis. In addition

phosphorylation levels of p-JNK

p-c-jun in the JNK pathway were markedly up-regulated. 【Conclusion】 Interleukin-17A might exacerbate insulin resistance through the activation of the JNK signaling pathway

and

resulted in aggravating fatty liver cells degeneration.