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【目的】研究胰岛素（insulin）急性刺激对PI3K/Akt和ERK信号的调节作用及其意义。【方法】HepG2细胞、6只8周龄BALB/C雄性小鼠分别都给予急性胰岛素刺激和磷酸盐缓冲液（PBS）刺激，细胞提取总蛋白、小鼠提取肝组织总蛋白用 Western blotting 法分析 Akt磷酸化水平和 ERK 磷酸化水平，并用免疫沉淀法检测TERT磷酸化水平。【结果】胰岛素急性刺激组 HepG2细胞和肝组织p-Akt、p-ERK水平均较PBS组上调，抑制PI3K/Akt信号通路后 TERT 活性下降。【结论】胰岛素急性刺激可以激活 PI3K/Akt和 ERK信号通路，抑制PI3K/Akt通路可减弱端粒酶活性，这可能为临床肝癌的诊断与治疗提供依据。“,”[Objective] To investigate the effect of acute insulin treatment on the regulation of PI 3K/Akt and ERK pathway and its significance .[Methods] HepG2 cells and 6 BALB /C male mice aged 8 weeks were treated with acute insulin and phosphate buffered saline (PBS) ,respectively .Total protein was extracted from cells and liver tissues in mice . Akt and ERK phosphorylation were examined by using Western blotting .Immunoprecipitation method was used to detect TERT phosphorylation .[Results]Compared with PBS group ,the levels of p-Akt and p-ERK in HepG2 cells and liver tissues of acute insulin treatment group were up-regulated .TERT activity was decreased after inhibiting PI3K/Akt signa-ling pathway .[Conclusion]Acute insulin treatment can activate PI3K/Akt and ERK pathway .Inhibition of PI3K pathway can decrease the activity of TERT ,which may provide the evidence for the diagnosis and treatment of liver cancer .