不同n-3/n-6多不饱和脂肪酸构成比膳食对大鼠一磷酸腺苷活化蛋白激酶表达的影响

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。

EFFECTS OF DIETARY DIFFERENT RATIOS OF n-3 TO n-6 POLYUNSATURATED FATTY ACIDS ON AMP-ACTIVATED PROTEIN KINASE EXPRESSION OF RATS

Objective To study the effects of dietary different ratios of n3/n6 polyunsaturated fatty acids(PUFA) on AMP-activated protein kinase (AMPK) expression of rats. Method According to serum total cholesterol level, male Sprague-Dawley rats were randomly divided into 6 groups, and fed common feed, high fat feed, high fat with n-3/n-6 1:1 PUFA feed, high fat with n-3/n-6 1:5 PUFA feed, common feed with n-3/n-6 1:1 PUFA diet and common feed with n-3/n-6 1:5 PUFA diet respectively. Weights were measured every 5 d, and food intakes were measured daily. We collected the blood sample at 0, 15, 30, 45 d and total cholesterol (TC) in the plasma were measured. After 45 d, the rats were sacrificed and Western blotting was used for measuring the expression of AMPK-a protein and its phosphorylation activity in liver and hypothalamus respectively. Results Four feeds with any ratio of n-3/n-6 PUFA resulted in significant decrease of body weight gain, TC in plasma, AMPK-a protein level in hypothalamus compared to high fat feeds. The AMPK-a protein level in liver increased in the four PUFA diets compared to high fat feeds. These situations in two groups with common feed were more significant than the high fat feed group. Conclusion Dietary PUFA improves lipid metabolism and decreases fat accumulation, which may be related with appetite control and fatty acid oxidation through AMPK path.