白介素-17A对胰岛素信号通路的影响及其机制

发布时间：2018-05-26 10:14

本文选题：白介素-A + 非酒精性脂肪性肝病　；参考：《中山大学学报(医学科学版)》2016年06期

【摘要】：【目的】研究白介素-17A在肝细胞脂肪变性的模型中对胰岛素抵抗的作用。【方法】用油酸诱导建立Hep G2细胞脂肪变性模型,在此模型中用白介素-17A作为干预物,研究白介素-17A对胰岛素信号通路的影响及机制。【结果】单纯IL-17A干预时,细胞p-AKT、p-PI3K磷酸化水平并没有明显变化,同时葡萄糖摄入、糖原合成p-GSK3β、糖异生p-FOXO1/G-6-pase/PEPCK和JNK通路上的p-JNK/p-c-jun等也未出现明显变化。而在高脂诱导Hep G2细胞变性模型中,白介素-17A的添加可促使胰岛素抵抗效应的产生,明显抑制细胞的胰岛素信号分子,p-AKT、p-PI3K磷酸化水平显著下降,同时还表现为葡萄糖摄入减少,糖原合成较少,糖异生增加。此外,JNK通路上的p-JNK、p-c-jun磷酸化水平显著升高。【结论】炎症因子白介素-17A可通过激活JNK通路,产生胰岛素抵抗效应,加剧肝细胞脂肪变性。
[Abstract]:[objective] to study the effect of interleukin-17A (IL-17A) on insulin resistance in hepatocyte steatosis model. [methods] A model of fatty degeneration of Hep G2 cells was established by oleic acid, in which interleukin-17A was used as an intervention. To study the effect of interleukin-17A on insulin signaling pathway and its mechanism. [results] the phosphorylation level of p-AKTN p-PI3K did not change, and glucose intake did not change. No significant changes were found in glycogen synthesis of p-GSK3 尾, glycosylated p-FOXO1/G-6-pase/PEPCK and p-JNK/p-c-jun in JNK pathway. In the model of hyperlipidemia induced denaturation of Hep G2 cells, the addition of interleukin-17A promoted the production of insulin resistance, and significantly decreased the phosphorylation level of p-AKTnp-PI3K, which also showed a decrease in glucose intake. The glycogen synthesis was less, and the glycometabolism increased. In addition, the phosphorylation level of p-JNKP p-c-jun in JNK pathway was significantly increased. [conclusion] Interleukin-17A can activate the JNK pathway and produce insulin resistance effect, thus exacerbating steatosis of hepatocytes.
【作者单位】：广东省膳食营养与健康重点实验室//中山大学公共卫生学院营养学系;
【基金】：国家重点基础研究发展计划(2012CB17506)
【分类号】：R575

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