中文摘要：

目的：研究抵抗素对肝细胞株HepG2葡萄糖代谢的影响,探讨抵抗素致糖尿病发生的可能机制。方法：50 ng/m L抵抗素作用HepG2肝细胞24 h,利用si RNA技术抑制HepG2细胞腺苷酸活化蛋白激酶（AMPK）α2亚基表达,实时定量RT-PCR技术检测葡萄糖代谢的相关基因AMPKα2、葡萄糖转运蛋白2（Glut2）、葡萄糖-6-磷酸酶（G6Pase）、磷酸烯醇式丙酮酸羧激酶（PEPCK）m RNA表达水平的变化,用Western blot检测AMPK磷酸化水平,液体闪烁技术检测肝细胞糖原的生成。结果 ：在基础及胰岛素刺激状态下,抵抗素降低肝细胞AMPKα2、Glut2 m RNA的表达及AMPK磷酸化水平（P〈0.05）,肝糖原合成减少（P〈0.05）,而G6Pase、PEPCK m RNA的表达增加（P〈0.05）。结论 ：抵抗素可通过AMPK途径影响葡萄糖代谢,使糖异生增加,而肝糖原合成减少,从而导致肝糖输出增多。

英文摘要：

Objective To investigate the effect of rh-resistin on glucose metabolism in HepG2 cells and to elucidate whether the underlying mechanisms are related to AMPK pathway. Methods Cells transfected with control si RNA or AMPKα2 si RNA were cultured in 6-well plates and then treated with 50 ng / m L rh-resistin for24 hours, while untransfected cells were treated with or without 50 ng / m L rh-resistin on the same conditions,followed by serum-starving in glucose-free DMEM for 3 ~ 5 hours in the continued absence or presence of rh-resistin. Then the cells were treated with or without insulin for 2 hours. AMPKα2, G6 Pase, PEPCK and Glut2 m RNA expression levels were determined by quantitative RT-PCR. The phosphorylation state of AMPK was determined by Western blotting. Glycogen synthesis was measured by the incorporation of D- [U-14C] glucose to glycogen. Results Rh-resistin suppressed the AMPKα2, Glut2 m RNA expressions, and reduced the phosphorylation level of AMPK and glycogen synthesis on both basal and insulin-stimulated conditions（P〈0.05）, while it accelerated G6 Pase and PEPCK m RNA expressions on the same conditions（P〈0.05）. The m RNA expression levels of G6 Pase, PEPCK, Glut2 and the phosphorylation level of AMPK and glycogen synthesis were significantly different between the rh-resistin group and the rh-resistin in conjunction with AMPKα2 si RNA-treated group. Conclusion Rh-resistin may affect glucose metabolism in HepG2 cell via AMPK pathway.