高脂饮食与小鼠/大鼠肠道微生态结构改变相关性的Meta分析
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摘要
目的系统评价高脂饮食与小鼠/大鼠肠道微生态结构改变的相关性。方法计算机检索PubMed、EMBASE、Cochrane图书馆、中国生物医学文献数据库、中国知网、维普期刊数据库、万方数据库,查找关于高脂饮食与肠道微生态相关性的随机对照研究。对纳入的研究利用RevMan 5.3进行Meta分析。结果共纳入研究15篇,皆是随机对照实验研究。Meta分析结果表明,高脂饮食小鼠/大鼠肠道双歧杆菌的含量减少(标准化均数差-4.08,95%可信区间-6.10～-2.05,P=0.000 1);高脂饮食对小鼠拟杆菌水平变化无明显差异(标准化均数差-0.5,95%可信区间-1.73～0.72,P=0.42),而高脂饮食的大鼠内拟杆菌明显减少(标准化均数差-1.46,95%可信区间-2.58～-0.35,P=0.01);同时肠道内乳酸杆菌的含量减少(标准化均数差-4.52,95%可信区间-7.39～-1.52,P<0.002);而肠道肠杆菌含量增加(标准化均数差3.93,95%可信区间0.53～7.32,P=0.02)。结果也表明高脂饮食后小鼠/大鼠体质量增加(标准化均数差3.74,95%可信区间2.81～4.67,P<0.000 01);血浆总胆固醇(标准化均数差3.52,95%可信区间2.39～4.65,P<0.000 01)及甘油三酯(标准化均数差1.87,95%可信区间1.14～2.60,P<0.000 01)在高脂饮食后均显著升高。结论高脂饮食可导致小鼠/大鼠肠道微生态结构的改变。肠道微生态结构改变可能在肥胖、高脂血症等代谢性疾病的发生中发挥重要作用。
Objective A meta analysis was made to review the relationship between high fat diet and the changes of intestinal microecology in mice/rats systematically. Methods Databases included PubMed,EMBASE,the Cochrane Library,China Biology Medicine disc,China National Knowledge Infrastructure,VIP database and Wanfang database were searched to collect the randomized controlled studies on the correlation between high fat diet and intestinal microecology. The meta analysis was performed using the RevMan 5.3. Results All of the 15 studies were randomized controlled trials. The results of meta analysis showed that intestinal bifidobacteria decreased after high fat diet(SMD-4.08,95%CI-6.10～-2.05,P=0.000 1). There was a decrease in intestinal bacteroides in mice/rats after high-fat diet(SMD-0.5,95% CI-1.73～0.72,P=0.42;SMD-1.46,95% CI-2.58～-0.35,P=0.01),and there was a significant decrease in intestinal lactobacillus as well(SMD-4.52,95%CI-7.39～-1.52,P<0.002). However,there was an increase in intestinal enterobacteriaceae in mice/rats after high-fat diet(SMD 3.93,95%CI 0.53～7.32,P=0.02). Also,the results showed that the weight of mice/rats increased after high-fat diet(SMD 3.74,95%CI 2.81～4.67,P<0.000 01). Concomitantly,the plasma total cholesterol(SMD 3.52,95%CI 2.39～4.65,P<0.000 01)and triglyceride(SMD 1.87,95%CI 1.14～2.60,P<0.000 01)in the mice/rats increased significantly after the high fat diet. Conclusion High fat diet can lead to the change of intestinal micro ecological structure in mice/rats. The change of intestinal micro ecological structure may play an important role in the pathogenesis of metabolic diseases such as obesity and hyperlipidemia.
Objective A meta analysis was made to review the relationship between high fat diet and the changes of intestinal microecology in mice/rats systematically. Methods Databases included PubMed,EMBASE,the Cochrane Library,China Biology Medicine disc,China National Knowledge Infrastructure,VIP database and Wanfang database were searched to collect the randomized controlled studies on the correlation between high fat diet and intestinal microecology. The meta analysis was performed using the RevMan 5.3. Results All of the 15 studies were randomized controlled trials. The results of meta analysis showed that intestinal bifidobacteria decreased after high fat diet(SMD-4.08,95%CI-6.10～-2.05,P=0.000 1). There was a decrease in intestinal bacteroides in mice/rats after high-fat diet(SMD-0.5,95% CI-1.73～0.72,P=0.42;SMD-1.46,95% CI-2.58～-0.35,P=0.01),and there was a significant decrease in intestinal lactobacillus as well(SMD-4.52,95%CI-7.39～-1.52,P<0.002). However,there was an increase in intestinal enterobacteriaceae in mice/rats after high-fat diet(SMD 3.93,95%CI 0.53～7.32,P=0.02). Also,the results showed that the weight of mice/rats increased after high-fat diet(SMD 3.74,95%CI 2.81～4.67,P<0.000 01). Concomitantly,the plasma total cholesterol(SMD 3.52,95%CI 2.39～4.65,P<0.000 01)and triglyceride(SMD 1.87,95%CI 1.14～2.60,P<0.000 01)in the mice/rats increased significantly after the high fat diet. Conclusion High fat diet can lead to the change of intestinal micro ecological structure in mice/rats. The change of intestinal micro ecological structure may play an important role in the pathogenesis of metabolic diseases such as obesity and hyperlipidemia.
引文
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[22]LI H,LELLIOTT C,HAKANSSON P,et al.Intestinal,adipose,and liver inflammation in diet-induced obese mice[J].Metabolism,2008,57(12):1704-1710.
[23]GOEL A,GUPTA M,AGGARWAL R.Gut microbiota and liver disease[J].J Gastroenterol Hepatol,2014,29(6):1139-1148.
[24]LI X M,JEFFERS L J,REDDY K R,et al.Immunophenotyping of lymphocytes in liver tissue of patients with chronic liver diseases by flow cytometry[J].Hepatology,1991,14(1):121-127.
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[27]CANI P D,DELZENNE N M.Interplay between obesity and associated metabolic disorders:New insights into the gut microbiota[J].Curr Opin Pharmacol,2009,9(6):737-743.
[28]BROWN J M,HAZEN S L.The gut microbial endocrine organ:Bacterially-derived signals driving cardiometabolic diseases[J].Annu Rev Med,2015,66:343-359.
[29]CANI P D,DELZENNE N M.The role of the gut microbiota in energy metabolism and metabolic disease[J].Curr Pharm Des,2009,15(13):1546-1558.
[30]LIN H V,FRASSETTO A,KOWALIK E J Jr.,et al.Butyrate and propionate protect against diet-induced obesity and regulate gut hormones via free fatty acid receptor 3-independent mechanisms[J].Plos One,2012,7(4):e35240.
[31]KIMURA I,OZAWA K,INOUE D,et al.The gut microbiota suppresses insulin-mediated fat accumulation via the shortchain fatty acid receptor GPR43[J].Nat Commun,2013,4(11):1829.
[32]TOLHURST G,HEFFRON H,YU S L,et al.Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein-coupled receptor FFAR2[J].Diabetes,2012,61(2):364-371.
[2]NG M,FLEMING T,ROBINSON M,et al.Global,regional,and national prevalence of overweight and obesity in children and adults during 1980-2013:A systematic analysis for the Global Burden of Disease Study 2013[J].Lancet,2014,384(9945):766-781.
[3]DUCA F,GéRARD P,COVASA M,et al.Metabolic interplay between gut bacteria and their host[J].Front Horm Res,2014,42:73-82.
[4]任婷婷,卢放根,张尤历,等.高脂饮食对SD大鼠肠道菌群的影响[J].世界华人消化杂志,2010,18(25):2694-2697.
[5]刘芳,高南南,杨润梅,等.不同品系小鼠肥胖模型比较及C57BL/6J小鼠肥胖机制研究[J].中国药理学通报,2013,29(3):360-365.
[6]王志凡,杨秀琳,陈旺盛,等.抗性淀粉对饮食诱导肥胖大鼠排便状况及肠道菌群的影响[J].动物营养学报,2016,28(5):1626-1632.
[7]姚瑛瑛,张峰,李艳琴,等.水杨酸铬(Ⅲ)配合物对肥胖小鼠肠道菌群的影响[J].食品与药品,2014,16(3):166-170.
[8]刘雪姬,陈庆森,闫亚丽.高脂饮食对小鼠肠道菌群的影响[J].食品科学,2011,32(23):306-311.
[9]曹战江,于健春,康维明,等.补充n-3多不饱和脂肪酸对高脂饮食大鼠肠道菌群及门静脉血内毒素的影响[J].中国医学科学院学报,2014,36(5):496-500.
[10]NEYRINCK A M,ALLIGIER M,MEMVANGA P B,et al.Curcuma longa extract associated with white pepper lessens high fat diet-induced inflammation in subcutaneous adipose tissue[J].PLoS One,2013,8(11):e81252.
[11]WANG J H,BOSE S,KIM G C,et al.Flos Lonicera ameliorates obesity and associated endotoxemia in rats through modulation of gut permeability and intestinal microbiota[J].PLoS One,2014,9(1):e86117.
[12]CANO P G,SANTACRUZ A,MOYAá,et al.Bacteroides uniformis CECT 7771 ameliorates metabolic and immunological dysfunction in mice with high-fat-diet induced obesity[J].PLoS One,2012,7(7):e41079.
[13]CANO P G,SANTACRUZ A,TREJO F M,et al.Bifidobacterium CECT 7765 improves metabolic and immunological alterations associated with obesity in high-fat diet-fed mice[J].Obesity(Silver Spring),2013,21(11):2310-2321.
[14]MOYA-PéREZ A,NEEF A,SANZ Y.Bifidobacterium pseudocatenulatum CECT 7765 reduces obesity-associated inflammation by restoring the lymphocyte-macrophage balance and gut microbiota structure in high-fat diet-fed mice[J].PLoSOne,2015,10(7):e0126976.
[15]WANG J H,BOSE S,KIM H G,et al.Fermented rhizoma atractylodis macrocephalae alleviates high fat diet-induced obesity in association with regulation of intestinal permeability and microbiota in rats[J].Sci Rep,2015,5:8391.
[16]DO T T,HINDLET P,WALIGORA-DUPRIET A J,et al.Disturbed intestinal nitrogen homeostasis in a mouse model of high-fat diet-induced obesity and glucose intolerance[J].Am JPhysiol Endocrinol Metab,2014,306(6):E668-680.
[17]CANI P D,NEYRINCK A M,FAVA F,et al.Selective increases of bifidobacteria in gut microflora improve high-fatdiet-induced diabetes in mice through a mechanism associated with endotoxaemia[J].Diabetologia,2007,50(11):2374-2383.
[18]CANI P D,BIBILONI R,KNAUF C,et al.Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice[J].Diabetes,2008,57(6):1470-1481.
[19]DELZENNE N M,NEYRINCK A M,BACKHED F,et al.Targeting gut microbiota in obesity:Effects of prebiotics and probiotics[J].Nat Rev Endocrinol,2011,7(11):639-646.
[20]DELZENNE N M,NEYRINCK A M,CANI P D.Gut microbiota and metabolic disorders:How prebiotic can work?[J].Br JNutr,2013,109(Suppl 2):S81-85.
[21]DELZENNE N M,NEYRINCK A M,CANI P D.Modulation of the gut microbiota by nutrients with prebiotic properties:Consequences for host health in the context of obesity and metabolic syndrome[J].Microb Cell Fact,2011,10(Suppl1):S10.
[22]LI H,LELLIOTT C,HAKANSSON P,et al.Intestinal,adipose,and liver inflammation in diet-induced obese mice[J].Metabolism,2008,57(12):1704-1710.
[23]GOEL A,GUPTA M,AGGARWAL R.Gut microbiota and liver disease[J].J Gastroenterol Hepatol,2014,29(6):1139-1148.
[24]LI X M,JEFFERS L J,REDDY K R,et al.Immunophenotyping of lymphocytes in liver tissue of patients with chronic liver diseases by flow cytometry[J].Hepatology,1991,14(1):121-127.
[25]BORST S E,CONOVER C F.High-fat diet induces increased tissue expression of TNF-alpha[J].Life Sci,2005,77(17):2156-2165.
[26]SANZ Y,RASTMANESH R,AGOSTONI C.Understanding the role of gut microbes and probiotics in obesity:How far are we?[J].Pharmacol Res,2013,69(1):144-155.
[27]CANI P D,DELZENNE N M.Interplay between obesity and associated metabolic disorders:New insights into the gut microbiota[J].Curr Opin Pharmacol,2009,9(6):737-743.
[28]BROWN J M,HAZEN S L.The gut microbial endocrine organ:Bacterially-derived signals driving cardiometabolic diseases[J].Annu Rev Med,2015,66:343-359.
[29]CANI P D,DELZENNE N M.The role of the gut microbiota in energy metabolism and metabolic disease[J].Curr Pharm Des,2009,15(13):1546-1558.
[30]LIN H V,FRASSETTO A,KOWALIK E J Jr.,et al.Butyrate and propionate protect against diet-induced obesity and regulate gut hormones via free fatty acid receptor 3-independent mechanisms[J].Plos One,2012,7(4):e35240.
[31]KIMURA I,OZAWA K,INOUE D,et al.The gut microbiota suppresses insulin-mediated fat accumulation via the shortchain fatty acid receptor GPR43[J].Nat Commun,2013,4(11):1829.
[32]TOLHURST G,HEFFRON H,YU S L,et al.Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein-coupled receptor FFAR2[J].Diabetes,2012,61(2):364-371.