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目的研究不同n-3/n-6配比脂肪酸对大鼠磷酸腺苷酸活化蛋白激酶(AMP-activated protein kinase,AMPK)蛋白及活性表达的影响。方法58只SD大鼠适应性喂养7d后,尾静脉取血。根据血清总胆固醇水平随机分为:空白(基础饲料);高脂(高脂饲料);高脂1:1(高脂饲料+n-3/n-6=1:1配方油);高脂1:5(高脂饲料+n3/n6=1:5配方油);低脂1:1(脱脂基础饲料+n-3/n-6=1:1配方油);低脂1:5(脱脂基础饲料+n3/n6=1:5配方油)6组,喂养45d,观察大鼠摄食与体重增长。于实验前1d,15d,30d,45d分别各取血测血清总胆固醇水平,于D45处死动物。Western blotting分别分析肝和下丘脑组织中AMPK-α总蛋白及其活性表达。结果添加PUFA的4个比例组血清TC、体重与高脂组相比,显著降低,且低脂2个比例组和高脂1:1组均与高脂1:5组相比有显著差异。添加PUFA的4个比例组均与高脂组相比,大鼠下丘脑AMPK-α总蛋白表达水平明显降低,肝AMPK-α蛋白表达水平均比高脂组明显升高。结论PUFA改善血脂可能是通过增加肝AMPK表达,抑制下丘脑AMPK表达,增加肝脂肪酸氧化和抑制食欲,影响血脂代谢。
Objective To investigate the effect of different n-3 / n-6 ratio of fatty acids on the protein and activity of AMPK in rats. Methods Fifty-eight SD rats were fed for 7 days. Blood was collected from tail vein. According to the level of serum total cholesterol, they were randomly divided into: blank (basal diet), high fat (high fat diet), high fat 1: 1 (high fat diet + n-3 / n-6 = Low fat 1: 1 (skim basic diet + n-3 / n-6 = 1: 1 formula oil); low fat 1: 5 Defatted basic diet + n3 / n6 = 1: 5 formula oil) 6 groups, fed 45d, to observe the rat feeding and weight gain. Serum total cholesterol levels were measured at 1 day, 15 days, 30 days and 45 days before the experiment, and animals were sacrificed at D45. The total protein and activity of AMPK-α in liver and hypothalamus were analyzed by Western blotting. Results Compared with the high-fat diet group, the serum TC levels of the four PUFA-supplemented groups were significantly lower than those of the high-fat diet group. There were significant differences between the low fat diet group and the high fat diet group in the 1: 5 high fat diet group. Compared with the hyperlipemia group, the expression of total AMPK-αprotein in the four proportions of PUFA-supplemented PUFA group was significantly lower than that of the high-fat group, and the level of AMPK-αprotein in liver tissue was significantly higher than that of the hyperlipemia group. Conclusions PUFA may improve blood lipid level by increasing hepatic AMPK expression, inhibiting hypothalamic AMPK expression, increasing hepatic fatty acid oxidation, suppressing appetite and affecting blood lipid metabolism.