Effect of Interleukin-17A on Insulin Signaling Pathway
LI Yan-ping;SHEN Tian-ran;CHEN Xu;LING Wen-hua;Guangdong Provincial Key Laboratory of Food,Nutrition and Health//Department of Nutrition, School of Public Health, Sun Yatsen University;
【Objective】To investigate the effect of interleukin-17 A on insulin resistance in hepatocyte steatosis model cells.【Methods】The model of hepatocyte steatosis in Hep G2 cells was generated by oleic-acid and then cells were treated with or without interleukin-17 A to classify its role in insulin signaling pathway. 【Results】No significant change was observed in p-AKT, p-PI3 K phosphorylation levels in Hep G2 cells treated with IL – 17 A 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 Hep G2 cells model, intervention with interleukin-17 A further induced insulin resistance effect, sharply inhibited cell insulin signaling molecules, and significantly decreased p-AKT, p-PI3 K 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-17 A might exacerbate insulin resistance through the activation of the JNK signaling pathway, and, resulted in aggravating fatty liver cells degeneration.
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