金丝桃苷对高脂饮食引起的肥胖伴胰岛素抵抗小鼠的保护作用

Protective effect of hyperoside on obese mice with insulin resistance induced by high-fat diet

目的研究金丝桃苷对高脂饮食引起的肥胖伴胰岛素抵抗小鼠的代谢保护作用。方法将30只C57BL/6小鼠随机分为对照组、高脂组及金丝桃苷组,对照组小鼠给予普通饲料,高脂组及金丝桃苷组给予高脂饲料,喂养14周后建模成功(n=10)。金丝桃苷组灌胃给予金丝桃苷,对照组给予溶媒,灌胃9周后收集血清,检测生化指标及细胞因子,qRT-PCR法检测肝脏内糖脂代谢相关基因,并观察肝脏形态。结果给予金丝桃苷后,金丝桃苷组小鼠的体重和空腹血糖较高脂组明显降低(P<0.05),且葡萄糖耐受能力显著增强(P<0.05)。金丝桃苷组小鼠的血清TC、TG、LDL及HDL水平显著低于高脂组(P<0.05),肝脏内脂质沉积也较高脂组减少,而脂联素和瘦素水平均明显高于高脂组(P<0.05)。与高脂组相比,金丝桃苷组小鼠SREBP1c、ACC、FAS基因表达降低,而AMPK基因表达增加(P<0.05)。结论金丝桃苷可降低高脂饮食小鼠的体重和血糖,改善胰岛素抵抗,抑制脂质合成,这些作用可能与AMPK及下游信号通路有关。

Objective To study the metabolic protective effect of hyperoside on obese mice with insulin resistance induced by high-fat diet.Methods Totally 30 C57BL/6 mice were randomly divided into control group,high-fat group and hyperoside group.Control group was given normal food,while HDF group and Hyp group were given high-fat food.The models were established(n=10)after 14 weeks of feeding,hyperoside was given by intragastric administration,and the solvent was given in control group.After 9 weeks of intragastric administration,the serum biochemical indexes and cytokines of the mice were detected,the expression of mRNAs related to glucose and lipid metabolism in liver was detected by qRT-PCR,and the morphology of liver was observed.Results After administration of hyperoside,the body weight and fasting blood glucose of mice in Hyp group were lower than those in HDF group(P<0.05),and the ability of glucose tolerance was significantly enhanced(P<0.05).The levels of serum TC,TG,LDL and HDL in Hyp group were lower than those in HDF group(P<0.05),and the lipid deposition in liver was also reduced,while the levels of adiponectin and leptin were significantly higher than those in HDF group(P<0.05).Compared with HDF group,the expression of SREBP1c,ACC and FAS genes in Hyp group was decreased,while the expression of AMPK gene increased significantly(P<0.05).Conclusion Hyperoside can reduce the body weight and blood glucose of mice fed with high-fat diet,improve the insulin resistance and inhibit the lipid synthesis,which may be related to AMPK and its downstream signaling pathway.