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目的探讨氯原酸(CGA)对胰岛素抵抗(IR)及高脂状态下糖代谢的调节作用。方法通过培养HepG2细胞,分别在正常、高胰岛素诱导肝细胞胰岛素抵抗以及油酸(OA)诱导脂肪变性状态下,给予不同剂量的CGA(10、20、40、80mg/L)共培养24h后,观察细胞形态学变化,用葡萄糖氧化酶法检测细胞的葡萄糖消耗量。结果在正常环境中,与对照组比较,CGA可显著增加细胞葡萄糖消耗量,且在10～40mg/L剂量范围内呈量效关系(P<0.05)。在胰岛素抵抗状态下,葡萄糖消耗量下降了39.5%(P<0.05);给予CGA后,细胞耗糖量较IR组增加了60.5%～93.5%(P<0.05),其中20mg/LCGA的作用最强。在脂肪变性状态下,葡萄糖消耗量下降了26.2%(P<0.05);给予CGA后,耗糖量较OA组增加了27.3%～63.5%(P<0.05),其中20mg/L组作用最强。结论CGA对高胰岛素和高脂诱导的糖代谢紊乱具有改善作用。
Objective To investigate the regulatory effect of chlorogenic acid (CGA) on glucose metabolism in insulin resistance (IR) and hyperlipidemia. Methods HepG2 cells were cultured and co-cultured with different doses of CGA (10, 20, 40 and 80 mg / L) for 24 h under normal and high insulin induced hepatocyte insulin resistance and oleic acid (OA) The morphological changes of cells were observed, and glucose oxidase method was used to detect the glucose consumption of cells. Results In normal environment, compared with the control group, CGA significantly increased cell glucose consumption, and dose-effect relationship in the dose range of 10 ~ 40mg / L (P <0.05). In the insulin resistance state, glucose consumption decreased by 39.5% (P <0.05). After CGA administration, the amount of glucose consumption increased by 60.5% -93.5% (P <0.05), and the effect of 20mg / LCGA Strong. In steatosis, glucose consumption decreased by 26.2% (P <0.05). After CGA administration, the amount of sugar consumption increased by 27.3% -63.5% (P <0.05) compared with OA group, and the effect of 20mg / L group was the strongest . Conclusions CGA can improve the disturbance of glucose metabolism induced by hyperinsulinemia and hyperlipidemia.