摘要
目的研究ATⅡ对人肝癌细胞株HepG2细胞葡萄糖代谢的影响,并探讨缬沙坦在该过程中的干预作用。方法体外培养HepG2细胞,分别加入10-9～10-5 mol/L的ATⅡ作用不同时间,确定对细胞葡萄糖消耗量影响最明显的ATⅡ浓度和作用时间。将HepG2细胞随机分为对照组、ATⅡ组、缬沙坦干预组,测定细胞葡萄糖消耗量、糖原合成量、糖异生量及糖酵解的指标。结果 10-6 mol/L的ATⅡ作用HepG2细胞36h,葡萄糖消耗量减少最明显(P<0.01)。ATⅡ作用后,细胞糖原合成量、乳酸生成量下降(P<0.05),糖异生量增加(P<0.05),丙酮酸激酶活力差异无统计学意义(P>0.05);缬沙坦干预后,糖异生量减少(P<0.05),糖原合成量增加(P<0.05)。结论缬沙坦可逆转ATⅡ所致的HepG2细胞葡萄糖代谢异常,为糖尿病预防及治疗提供参考。
Objective To investigate the effect of ATII on glucose metabolism in HepG2 ceils, and to observe the intervention of valsartan on it. Methods Different concentrations of AT lI （10^-9-10^-5mol/L） were added into the cultured HepG2 cells for different times, and the amount of glucose consumption was measured. The time and concentration of AT Ⅱ affecting glucose metabolism were determined. Then the HepG2 cells were randomized into the control group, AT Ⅱ group, and valsartan pretreated group. The glycogenesis, gluconeogenesis and glycolysis in HepG2 cells were measured. Results The best time and concentration of ATⅡ were at 36 h and 10-^-5mol/L. ATⅡ decreased glucose consumption through decreasing the glyeogenesis and lactic acid production and increasing gluconeogenesis, while no significant impact on pyruvate kinase activity. Valsartan could antagonize ATⅡ ＇s effect mainly through the inhibition of gluconeogenesis and promotion of glycogenesis. Conclusion Valsartan can reverse the effect of AT IX on glucose metabolism, providing a theoretical basis for the prevention and treatment of diabetes.
出处
《中国糖尿病杂志》
CAS
CSCD
北大核心
2013年第6期555-557,共3页
Chinese Journal of Diabetes
关键词
血管紧张素Ⅱ
缬沙坦
葡萄糖消耗
糖原合成
糖异生
Angiotensin Ⅱ（ATⅡ）
Valsartan） Glucose consumption
Glycogenesis
Gluconeogenesis
