为研究苦瓜水提物（BMWE）和醇提物（BMEE）调节胰岛素抵抗的异同点，本文采用棕榈酸诱导HepG2细胞建立胰岛素抵抗（IR）细胞模型，测定了BMWE和BMEE对HepG2-IR细胞葡萄糖消耗量、糖原、甘油三酯（TG）、ATP及胰岛素抵抗信号通路相关基因mRNA表达水平的影响。结果表明，BMWE和BMEE均可显著增加IR细胞的葡萄糖消耗量和胞内糖原含量；BMEE还能显著降低细胞中TG含量（112.08% vs. 132.97%）、增加细胞中ATP含量（80.62% vs. 48.44%）；同时BMWE和BMEE均能显著提高IR细胞中IRS1（胰岛素受体1）、PI3K（磷脂酰肌醇-3-激酶）、AMPK（腺苷酸活化蛋白激酶）和CPT1（肉毒碱棕榈酰转移酶1）mRNA的表达水平，降低ACC2（乙酰辅酶A羟化酶2）mRNA的表达水平；BMWE还可增加细胞中AKT（蛋白激酶B）mRNA的表达水平。在mRNA水平，BMWE通过激活IR细胞的IRS1-PI3K-AKT信号通路改善胰岛素抵抗；而BMEE则通过调节AMPK-ACC2-CPT1信号通路改善IR细胞的糖脂代谢，二者的作用途径有所不同。

In order to investigate the similarities and differences in the regulation of insulin resistance between water extracts (BMWE) and ethanol extracts (BMEE) from bitter melon on insulin resistant, the insulin resistance (IR) cell model was established in HepG2 cells induced by palmitic acid. Glucose consumption, glycogen, triglyceride (TG), ATP content and the mRNA expression levels of relative gene were determined. The results showed that BMWE and BMEE could significantly increase the glucose consumption and intracellular glycogen content of IR cells, and BMEE could significantly decrease TG content in cells (112.08% vs. 132.97%) and increase ATP content in cells (80.62% vs. 48.44%); BMWE and BMEE could increase insulin receptor substrate 1 (IRS1), phosphatidylinositol 3-kinase (PI3K), adenosine 5‘-monophosphate -activated protein kinase (AMPK) and carnitine palmitoyltransferase 1 (CPT1) mRNA expression, and could decrease acetyl-CoA carboxylase 2 (ACC2) mRNA expression; BMWE could also increase protein kinase B (AKT) mRNA expression. BMWE might improve insulin resistance by activating IRS1-PI3K-AKT signaling pathway in IR cells; However, BMEE could regulate glucose and lipid metabolism of IR cells through AMPK-ACC2-CPT1 signaling pathway, and their action pathways were different.

国家自然科学基金项目（31371760）；江苏高校优势学科建设工程项目；江苏大学高级人才科研启动基金项目（15JDG065）；镇江市重点研发项目（现代农业）（NY2017009）