Wu Mianyun, Wang Ximing, Duan Qiuhong, Lu Tao
Biochemistry Department, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ann Nutr Metab. 2007;51(3):270-6. doi: 10.1159/000105448. Epub 2007 Jul 9.
To investigate whole-body metabolic disorder and hepatic glucose output (HGO) disturbance in rats with insulin resistance induced by a short-term high-fat diet, and the effect of arachidonic acid (AA).
Twenty-four normal male Wistar rats (230-250 g) were randomly divided into 3 groups according to their weight and fed for 12 weeks: control group, n = 8, fed with standard chow diet; high-fat (HF) group, n = 8, fed with a high-fat diet; HF+AA group, n = 8, fed with a high-fat diet and administered orally 3 mg x kg(-1) x day(-1)AA.
Early insulin resistance was successfully induced in HF-fed rats with hyperinsulinemia (p < 0.05), higher plasma triglyceride (TG) (p < 0.05), higher fasting liver glycogen content (p < 0.01) and higher glucose-insulin index (p < 0.01) during an oral glucose tolerance test (OGTT). The AA treatment significantly decreased the glucose-insulin index (p < 0.01), blood TG (p < 0.05) and glycogen content (p < 0.05) in liver. Both activity of phosphoenolpyruvate carboxykinase (PEPCK) (p < 0.05) and mRNA levels of PEPCK (p < 0.05) and glucose-6-phosphatase (G-6-Pase) (p < 0.01) in liver were also observed to be significantly decreased. But there were significant differences in the glucose-insulin index (p < 0.01) during OGTT, and glycogen content (p < 0.01) between the HF+AA and control groups.
AA can significantly prevent whole-body insulin resistance induced by a high-fat diet, as well as accompanied HGO disturbance in the overnight fasting state, but not thoroughly.
研究短期高脂饮食诱导的胰岛素抵抗大鼠的全身代谢紊乱及肝葡萄糖输出（HGO）障碍，以及花生四烯酸（AA）的作用。
将24只体重为230 - 250 g的正常雄性Wistar大鼠按体重随机分为3组，喂养12周：对照组，n = 8，喂标准普通饲料；高脂（HF）组，n = 8，喂高脂饮食；HF + AA组，n = 8，喂高脂饮食并口服3 mg·kg⁻¹·d⁻¹ AA。
高脂喂养的大鼠成功诱导出早期胰岛素抵抗，伴有高胰岛素血症（p < 0.05）、较高的血浆甘油三酯（TG）（p < 0.05）、较高的空腹肝糖原含量（p < 0.01）以及口服葡萄糖耐量试验（OGTT）期间较高的葡萄糖 - 胰岛素指数（p < 0.01）。AA治疗显著降低了葡萄糖 - 胰岛素指数（p < 0.01）、血液TG（p < 0.05）和肝脏糖原含量（p < 0.05）。还观察到肝脏中磷酸烯醇式丙酮酸羧激酶（PEPCK）的活性（p < 0.05）以及PEPCK的mRNA水平（p < 0.05）和葡萄糖 - 6 - 磷酸酶（G - 6 - Pase）的mRNA水平（p < 0.01）均显著降低。但HF + AA组与对照组在OGTT期间的葡萄糖 - 胰岛素指数（p < 0.01）以及糖原含量（p < 0.01）方面存在显著差异。
AA可显著预防高脂饮食诱导的全身胰岛素抵抗以及空腹状态下伴随的HGO障碍，但不能完全预防。
