摘要
目的观察槲皮素-3-o-新橙皮糖苷对L6肌管细胞胰岛素抵抗模型葡萄糖消耗;脂肪酸消耗以及对PPARα、PPARγ、GLUT4表达量的调节作用及其作用机制。方法以250μmol/L的脂肪酸诱导形成L6肌管细胞胰岛素抵抗模型,以槲皮素-3-o-新橙皮糖苷干预24 h后,葡萄糖氧化酶法检测葡萄糖消耗量,气相色谱法(GC)检测脂肪酸消耗量,Western-blot方法检测细胞中葡萄糖转运蛋白4(GLUT4)以及PPARα、PPARγ的表达量。结果槲皮素-3-o-新橙皮糖苷处理可提高L6细胞对葡萄糖的消耗(P<0.01),降低细胞脂肪酸摄入(P<0.05),上调GLUT4和PPARγ蛋白表达量(分别为P<0.01和P<0.05),但对PPARα的表达量无明显影响。结论槲皮素-3-o-新橙皮糖苷可提高L6细胞胰岛素抵抗模型葡萄糖消耗量,降低脂肪酸摄入,调节PPARγ、GLUT4的表达,这些可能是受试物缓解胰岛素抵抗的机制之一。
Objective To detect the effect of quercetin-3-o-neohesperidin on glucose consumption and fatty acid consumption and the expression of PPARα,PPAR,GLUT4 in L6 insulin resistance cell model,and then analyze its molecular mechanism.Methods The L6 myotube cells were derivated by 250 μmol/L free fatty acid to establish the insulin resistance cell model,then were intervened by quercetin-3-o-neohesperidin for 24 h.The glucose consumption and fatty acid consumption were measured by glucose oxidase method and GC respectively.The expression of GLUT4,PPARα,PPARγ were detected by Western-blot.Results Quercetin-3-o-neohesperidin increased the glucose consumption(P<0.01) and decreased the fatty acid consumption(P<0.05) in L6 cells,and up-regulated the protein expression of GLUT4,PPARγ(P<0.01,P<0.05 respectively).However,quercetin-3-o-neohesperidin did not show any significant impact on the expression of PPARα between groups.Conclusion Quercetin-3-o-neohesperidin increase glucose consumption and decrease the fatty acid consumption in L6 insulin resistance cell model,up-regulate the protein expression of GLUT4 and PPARγ.Quercetin-3-o-neohesperidin plays a potential hypoglycemic and insulin sensitivity-improving effect.
出处
《食品安全质量检测学报》
CAS
2013年第3期813-818,共6页
Journal of Food Safety and Quality
基金
浙江省医药卫生平台重点资助计划(2011ZDA001)
浙江省科技计划项目(2009R50028
2011F20038
2011R09028-09)
浙江省151人才培养项目
浙江省营养学医学支撑学科建设~~
