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血管紧张素Ⅱ对人肝癌细胞株HepG2细胞葡萄糖代谢的影响及缬沙坦干预作用的研究

来自:中国糖尿病杂志  编辑:唐丽 高率斌 王丹萍|点击数:|2013-06-24

  ·糖尿病基础研究·


  【摘要】 目的 研究血管紧张素Ⅱ(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10-5 mol/L到10-9 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,继而将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36 h,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。

  【关键词】 血管紧张素Ⅱ;缬沙坦;葡萄糖消耗;糖原合成;糖异生

Effect of angiotensinⅡon glucose metabolism in HepG2 cells and intervention of valsartan on it TANG Li, GAO Shuai-bin, WANG Dan-ping ,et al. Department of Endocrinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China

Corresponding author: LI Xia-lian, E-mail: xialianli@hotmail.com

  【Abstract】 Objective To investigate the effect of ATⅡ on glucose metabolism in HepG2 cells, and to observe the intervention of valsartan on it. Methods Different concentrations of ATⅡ (10-5~10-9 mol/L) were added into the cultured HepG2 cells for different times, and the amount of glucose consumption was measured. The time and concentration of ATⅡ that affected markedly were determined. Then the HepG2 cells were randomized into the control group, ATⅡgroup, and valsartan pretreated group. The glycogenesis, gluconeogenesis and glycolysis in HepG2 cells were measured. Results The best time and concentration of ATⅡ were at 36h and 10-6 mol/L. ATⅡ decreased glucose consumption through decreasing the glycogenesis 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 ATⅡ on glucose metabolism, providing a theoretical basis for the prevention and treatment of diabetes.

  【Key words】 AngiotensinⅡ; Valsartan; Glucose consumption; Glycogenesis; Gluconeogenesis

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