【打印本页】 【下载PDF全文】 【HTML】 查看/发表评论下载PDF阅读器关闭

←前一篇|后一篇→

过刊浏览    高级检索

本文已被:浏览 1577次   下载 1306 本文二维码信息
码上扫一扫!
植物甾醇酯对高脂饮食诱导非酒精性脂肪肝病大鼠血清氨基酸谱的影响
周海玥1,管玘1,桂娟2,欧阳鹏凌1,丁信文1,马莉3,宋立华1*
0
(1. 上海交通大学农业与生物学院食品科学与工程系, 上海 200240;
2. 上海交通大学分析测试中心, 上海 200240;
3. 上海中医药大学附属岳阳中西医结合医院营养科, 上海 200437
*通信作者)
摘要:
目的 研究植物甾醇酯(PSE)对高脂饮食诱导非酒精性脂肪肝病(NAFLD)大鼠肝脂肪变性及血清氨基酸谱的影响。方法 实验将31只雄性SD大鼠分为正常对照组(NC组,n=7)、单纯高脂饮食组(HF组,n=12)及PSE干预组(PSE+HF组,n=12)。HF组和PSE+HF组大鼠以高脂饮食造模,PSE+HF组大鼠饲喂高脂饮食的同时连续灌胃给予PSE 0.5 g/kg,干预时间为12周。油红O染色观察高脂饮食作用下PSE对肝组织脂肪变性的影响,用氨基酸自动分析仪检测血清氨基酸谱情况。利用Pearson相关性分析判断各氨基酸与肝脏脂肪变性程度的相关性,利用SIMCA-P 11.5软件进行偏最小二乘法-判别分析(PLS-DA)。结果 PSE+HF组与HF组大鼠体质量差异无统计学意义(P>0.05),且NC、HF、PSE+HF 3组大鼠摄食量差异无统计学意义(P>0.05)。肝组织油红O染色结果表明,与HF组相比,PSE+HF组大鼠肝组织脂肪变性程度减轻。PSE+HF组血清必需氨基酸异亮氨酸、亮氨酸和非必需氨基酸半胱氨酸、天冬氨酸、谷氨酸、丙氨酸含量分别较HF组增加了17.25%、12.42%、41.47%、15.61%、17.87%、16.07%,差异均有统计学意义(P均<0.05);血氨及组氨酸水平均较HF组降低(P均<0.05)。PLS-DA分析结果显示HF组与PSE+HF组可分别聚类。Pearson相关性分析结果表明,组氨酸、脯氨酸及血氨水平与肝脏脂肪变性程度呈正相关(P均<0.01),色氨酸、苯丙氨酸、异亮氨酸、半胱氨酸、谷氨酸及相关代谢物鸟氨酸与肝脏脂肪变性程度呈负相关(P均<0.05)。结论 PSE对NAFLD大鼠血氨基酸代谢谱具有调节作用。
关键词:  植物甾醇酯  非酒精性脂肪肝病  脂肪变性  氨基酸
DOI:10.16781/j.0258-879x.2018.10.1115
投稿时间:2018-01-03修订日期:2018-04-16
基金项目:巴斯夫Newtrition®亚洲研究基金(14H100000490).
Effects of phytosterol ester on amino acid profile of rats with non-alcoholic fatty liver disease induced by high fat diet
ZHOU Hai-yue1,GUAN Qi1,GUI Juan2,OUYANG Peng-ling1,DING Xin-wen1,MA Li3,SONG Li-hua1*
(1. Department of Food Science and Engineering, Shanghai Jiao Tong University School of Agriculture and Biology, Shanghai 200240, China;
2. Instrumental Analysis Center, Shanghai Jiao Tong University, Shanghai 200240, China;
3. Department of Nutriology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200437, China
*Corresponding author)
Abstract:
Objective To explore the effects of phytosterol ester (PSE) on the hepatic steatosis and amino acid profile of rats with non-alcoholic fatty liver disease (NAFLD) induced by high fat diet. Methods Thirty-one male SD rats were randomly divided into normal control group (NC group, n=7), high fat diet group (HF group, n=12) and PSE intervention group (PSE+HF group, n=12). The rats in the HF and PSE+HF groups were fed with high-fat diet to establish the NAFLD rat model, and the rats in the PSE+HF group were continuously intragastrically administered with PSE 0.5 g/kg for 12 weeks. The hepatic steatosis was evaluated with Oil Red O staining, and the serum amino acid profile was analyzed using automatic amino acid analyzer. Pearson correlation analysis was used to investigate the correlation between amino acids and degree of liver steatosis. Partial least squares-discriminant analysis (PLS-DA) was carried out using SIMCA-P 11.5 software. Results There was no significant difference in body mass of rats between the PSE+HF group and HF group (P>0.05). Moreover, there was no significant difference in food intake of rats between the NC, HF and PSE+HF groups (P>0.05). Compared with the HF group, the hepatic steatosis of rats was partly alleviated in the PSE+HF group. The serum levels of essential amino acids, including isoleucine and leucine, and the non-essential amino acids, including cysteine, aspartate, glutamate and alanine, in the PSE+HF group were increased by 17.25%, 12.42%, 41.47%, 15.61%, 17.87% and 16.07%, respectively, compared with the HF group, and the differences were statistically significant (all P<0.05). The levels of serum NH3 and histidine were significantly decreased in the PSE+HF group versus the HF group (both P<0.05). PLS-DA analysis results showed that HF group and PSE+HF group could be clustered respectively. Pearson correlation analysis results showed that the levels of histidine, proline and serum NH3 were positively correlated with the degree of hepatic steatosis (all P<0.01); and tryptophan, phenylalanine, isoleucine, cysteine, glutamate and the related metabolites, ornithine, were negatively correlated with the degree of hepatic steatosis (all P<0.05). Conclusion PSE can regulate the amino acid metabolic profile of rats with NAFLD induced by high fat diet.
Key words:  phytosterol ester  non-alcoholic fatty liver disease  hepatic steatosis  amino acids