当前位置:主页 > 医学论文 > 内分泌论文 >

富硒益生菌对高脂肪日粮小鼠脂代谢、抗氧化状态、组织病理学损伤和生化指标的影响

发布时间:2018-05-05 07:48

  本文选题:富硒益生菌 + 肥胖 ; 参考:《南京农业大学》2015年硕士论文


【摘要】:在过去的几十年里,肥胖及其并发症的发生率在全球范围内大大增加了。其原因除了食物摄入的增多和体力活动的减少,越来越多的证据表明胃肠道中的微生物(即肠道菌群)与肥胖症的发生和相关代谢息息相关。微量元素硒是人和动物重要的的必须营养素。由于许多国家的饮食中硒往往低于最佳含量,因此通过在食物中补充或强化硒的添加已经越来越普遍。市售硒补充剂包括无机矿物盐(例如亚硒酸钠和硒酸盐)和有机硒(如富硒酵母)。研究目的这项研究的目的是评估富硒益生菌(SP)对高脂肪饮食(HFD)老鼠的脂类代谢,抗氧化状态,组织病理学损伤和生化指标的影响。试验设计80只4周龄,平均体重23克的雌性白化ICR老鼠被随机分成5个组(n=16)。A组老鼠饲喂正常饲料作为阴性对照组,B组老鼠饲喂HFD(15%)作为阳性对照组,C组老鼠饲喂HFD的同时给予益生菌(P,包含嗜酸乳杆菌1011/mL CFU和酿酒酵母菌109/mLCFU),D组和E组老鼠分别饲喂HFD的同时给予亚硒酸钠(SS)/SP(折算的硒含量都为0.3μg/g)。基础饮食的硒含量以国家研究委员会(NRC,1995)制定的0.05 mg/kg为标准。根据动物实验室和南京农业大学动物福利委员会(经江苏省科学技术厅批准)的要求饲养动物并开展动物试验。老鼠被安置在室温25±2℃的室内,并提供12小时黑暗/12小时光照。用于本研究的SP和P中包含两个益生菌菌株,嗜酸乳杆菌1011/mL(CFU)和酿酒酵母菌109/mL(CFU)。使用AF-610原子荧光光谱仪进行检测,SP中的硒含量为10.0 mg/L,且其中大于90%是有机硒,大于75%是硒代蛋氨酸。C组和E组中益生菌的量是相同的,嗜酸乳杆菌为0.25*1011/mL(CFU),酿酒酵母菌为0.25*109/mL(CFU)。SP和SS与高脂肪日粮混匀后碾成粉末。检测总蛋白(TP)、总胆固醇(TC)、丙氨酸转氨酶(AST)、天门冬氨酸转氨酶(ALT)的水平。LDL,HDL和TG试剂盒由南京建成生物工程研究所提供。测定GSH-Px,SOD,CAT活性和MDA水平。为了确定SP影响脂质内稳态机制,我们分析了与脂质代谢相关基因的mRNA水平(CPT1,CPT2,ACOX2,ACAT2,FAS,LPL,PPARα,PPARγ and SREBP2)。引物序列是通过Primer 5.0在线软件设计的,序列见表1。在试验的结束时(第5周)采集老鼠血液和肝脏样品,用于检测脂质代谢、抗氧化状态、病理学变化和相关基因的表达。试验结果B组老鼠的体重比其他几个组(A,C,D和E)大。肝组织的病理学检查表明,与B组相比C,D,E组的肝组织损伤更小,肝细胞内的脂肪空泡更少。C,D,E组的血清AST,ALT,TC,TG和LDL-C比B组显著下降,TP和HDL-C比B组显著上升。C,D,E组的SOD,CAT和GSH-Px酶活性比B组显著提高,MDA水平则比B.组显著下降。与B组相比,C,D,E组缓解了肝细胞内脂质的堆积。大体而言,添加P,SS或 SP 上调了 CPT1,CPT2,ACAT2 ACOX2 和 PPARα 的 mRNA 表达水平,下调了FAS,LPL,PPARy和SREBP1的mRNA表达水平,这些基因都参与了脂质的代谢。在这几组中,增加SP对改善高脂饮食老鼠的脂质代谢,抗氧化状态,病理学变化和相关基因表达的效果最理想。结论高脂饮食可以显著促进肥胖、氧化应激的发生,造成脂质重分布。而益生菌、富硒益生菌和亚硒酸钠可以显著改善高脂饮食诱导肥胖老鼠的脂质分布、氧化状态和相关基因的表达。
[Abstract]:In the past few decades, the incidence of obesity and its complications has increased worldwide. In addition to the increase in food intake and decrease in physical activity, more and more evidence suggests that microorganisms in the gastrointestinal tract (intestinal flora) are associated with obesity and related metabolism. Trace elements selenium is human and active. Important nutrients are essential. As selenium is often lower in the diet of many countries, it is becoming more and more common to add or strengthen selenium in food. The market selenium supplements include inorganic mineral salts (such as sodium selenite and selenate) and organic selenium (such as selenium enriched yeast). The purpose of this study is to study the purpose of this study The effects of selenium enriched probiotics (SP) on lipid metabolism, antioxidant status, histopathological damage and biochemical indexes in high fat diet (HFD) mice were evaluated. 80 4 weeks old female albino ICR mice with an average weight of 23 grams were randomly divided into 5 groups (n=16) group.A rats fed normal diet as negative control group, and B group mice fed HFD (15). As a positive control group, group C rats were fed HFD with probiotics (P, including Lactobacillus acidophilus 1011/mL CFU and Saccharomyces cerevisiae 109/mLCFU), D group and E group were fed HFD (SS) /SP (SS) /SP (0.3 mu g/g). The selenium content of basic diet was formulated by National Research Committee (1995) 0.05 mg/kg was the standard. Animals were raised in accordance with animal laboratories and the animal welfare committee of Nanjing Agricultural University (approved by the Jiangsu Department of science and Technology). Animals were fed and conducted animal tests. Mice were placed in room at room temperature of 25 + 2 and provided 12 hours of dark /12. Two probiotic strains were included in the study's SP and P. Lactobacillus acidophilus 1011/mL (CFU) and Saccharomyces cerevisiae 109/mL (CFU) were detected by AF-610 atomic fluorescence spectrometer. The selenium content in SP was 10 mg/L, and more than 90% was organic selenium, and greater than 75% was the same amount of probiotics in the selenium methionine.C group and the E group, and the Lactobacillus acidophilus was 0.25*1011/mL (CFU) and the Saccharomyces cerevisiae was 0.25*109/mL. (CFU).SP and SS were mixed with high fat diet to powder. The total protein (TP), total cholesterol (TC), alanine aminotransferase (AST), the level.LDL of aspartate aminotransferase (ALT), HDL and TG kits were provided by the Institute of bioengineering in Nanjing. We analyzed the mRNA levels of lipid metabolism related genes (CPT1, CPT2, ACOX2, ACAT2, FAS, LPL, PPAR a, PPAR gamma and SREBP2). The primer sequence was designed through the Primer 5 online software. The sequence was shown in table 1. to collect blood and liver samples at the end of the test (fifth weeks) for the detection of lipid metabolism, antioxidant status, and pathological changes. The body weight of the B group was larger than that of the other groups (A, C, D and E). The pathological examination of the liver tissue showed that the liver tissues of the group of C, D, and E were smaller than the B group, and the lipid vacuoles in the liver cells were less.C, D. The activity of SOD, CAT and GSH-Px was significantly higher than that in the B group, while the MDA level was significantly lower than that in the B. group. The levels of C, D, E groups relieved the accumulation of lipid in the liver cells. In these groups, increasing SP has the best effect on improving lipid metabolism, antioxidant status, pathological changes and related gene expression in high fat diet mice. Conclusion high fat diet can significantly promote obesity, oxidative stress and lipid redistribution, while probiotics, selenium enriched probiotics and sodium selenite can be used. To significantly improve lipid distribution, oxidative status and related gene expression in obese rats induced by high-fat diet.

【学位授予单位】:南京农业大学
【学位级别】:硕士
【学位授予年份】:2015
【分类号】:S816;R589.2

【参考文献】

相关期刊论文 前2条

1 Stephan Ebner;Linda N Smug;Wolfgang Kneifel;Seppo J Salminen;Mary Ellen Sanders;;Probiotics in dietary guidelines and clinical recommendations outside the European Union[J];World Journal of Gastroenterology;2014年43期

2 ;Protective effect of selenium-enriched lactobacilluson CCI_4-induced liver injury in mice and its possible mechanisms[J];World Journal of Gastroenterology;2005年37期



本文编号:1846824

资料下载
论文发表

本文链接:https://www.wllwen.com/yixuelunwen/nfm/1846824.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户8fde8***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com