氯原酸对高胰岛素与高油酸状态下HepG2细胞葡萄糖利用的影响

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。

EFFECT OF CHLOROGENIC ACID ON GLUCOSE CONSUMPTION IN HepG2 CELLS PRETREATED WITH HIGH INSULIN AND HIGH OLEIC ACID

Objective To explore the modulation of chlorogenic acid (CGA) on glucose metabolism in HepG2 cells pretreated with high insulin and high oleic acid (OA). Methods Cultured HepG2 cells induced by high insulin and oleic acid for insulin resistance and steatosis respectively, were co-cultured with different concentrations of CGA (10, 20, 40, 80 mg/L) for 24h. The morphological changes were observed and glucose consumptions of cells were measured by glucose oxidase method. Results Compared to control group, CGA could significantly increase glucose consumption of normal HepG2 cells and the dose-dependent effect was noted between 10-40 mg/L(P<0.05). The glucose consumption of HepG2 cells in insulin resistance (IR) group was decreased by 39.5% (P<0.05), but increased by 60.5%-93.5% as compared to IR group (P<0.05), after the cells were treated by CGA, most potent in 20mg/L CGA group. The glucose consumption of HepG2 cells in OA group was decreased by 26.2% (P<0.05), but increased by 27.3%-63.5% as compared to OA group (P<0.05), after the cells were treated by CGA, also most potent in 20 mg/L CGA group. Conclusion CGA can improve glucose metabolic disturbance induced by high insulin and high oleic acid.