中文摘要：

目的研究绿原酸对高脂饲喂SD大鼠骨骼肌糖代谢的调节机制。方法 40只雄性SD大鼠随机分成5组：对照组、模型组,低、高剂量（20、90 mg/kg）绿原酸组,罗格列酮（阳性对照）组,其中对照组饲喂普通饲料,其余各组大鼠饲喂高脂饲料。给药12周后处死大鼠,取骨骼肌,用实时荧光定量-PCR方法测定骨骼肌糖代谢过程中相关基因蛋白激酶B（PKB,又名Akt）、磷脂酰肌醇-3激酶（PI3K）、胰岛素受体底物-1（IRS-1）、葡萄糖转运蛋白4（GLUT-4）、蛋白激酶A（PKA）、AMP依赖的蛋白激酶（AMPK-α2）、过氧化物酶体增殖物激活受体（PPARα、PPARβ、PPARγ）的表达。结果与对照组比较,模型组大鼠骨骼肌中GLUT-4、AMPK-α2和PPARβm RNA表达量显著下降（P〈0.05、0.01）;与模型组相比,绿原酸干预能提高糖代谢途径中相关基因的表达,其中绿原酸高剂量组Akt、PI3K、IRS-1、GLUT-4、PKA、AMPK-α2、PPARα、PPARβm RNA的表达量显著上调（P〈0.05、0.01）。结论高剂量绿原酸能显著减缓高脂饲喂SD大鼠体质量增加,并通过调节PI3K/Akt途径、AMPK途径和胰岛素敏感性,改善骨骼肌中糖代谢。

英文摘要：

Objective To investigate the mechanisms of chlorogenic acid（CGA） on regulating carbohydrate metabolism in skeletal muscle of SD rats fed on high-fat diet. Methods Forty male SD rats were randomly divided into five groups： normal control（NC）, high-fat diet（HFD）, HFD with low-dose-CGA（20 mg/kg, HFD-LC）, HFD with high-dose-CGA（90 mg/kg, HFD-HC）, and Rosiglitazone（HFD-ROS） groups. NC rats were fed with normal chow diet, while the other rats were fed with HFD. The rats were killed after 12 weeks, and the real-time PCR method was used to measure the expression levels of GLUT-4, PKA, Akt, AMPKα2, IRS-1, PI3 K, and PPARs m RNA in skeletal muscle. Results The expression levels of GLUT-4, AMPKα2, and PPARβ in HFD group were more dramatically decreased than those in the NC group（P 0.05）; Compared with the HFD group, CGA increased genes involved in carbohydrate metabolism, particularly Akt, PI3 K, IRS-1, GLUT-4, PKA, AMPKα2, PPARα, and PPARβ in HFD-HC group（P 0.05）. Conclusion High-dose CGA could significantly slow the weight gain induced by HFD, as well as improve carbohydrate metabolism in skeletal muscle through regulating PI3K/Akt and AMPK signaling pathways, and insulin sensitivity.