Significant correlation between relieving of non-alcoholic fatty liver disease and regulation on gut microbiota and short-chain fatty acids in mice by Lactobacillus reuteri CCFM8631

  • JIAO Ting ,
  • ZHU Huiyue ,
  • SI Qian ,
  • XU Mengshu ,
  • SUN Shanshan ,
  • MA Fangli ,
  • WANG Gang ,
  • ZHAO Jianxin ,
  • ZHANG Hao ,
  • CHEN Wei
Expand
  • 1(School of Food Science and Technology, Jiangnan University, Wuxi 214122, China)
    2(Infinitus (China) Company Ltd., Guangzhou 510623, China)

Received date: 2020-01-06

  Online published: 2020-06-17

Abstract

In order to investigate the effects of different lactic acid bacteria (LAB) on the progression of non-alcoholic fatty liver disease (NAFLD) in mice which was induced by a high-fat and high-cholesterol diet (HFHCD), 4-week-old C57BL/6J mice were fed with HFHCD while administrated different LAB for 23 weeks. At the end of experiment, the blood lipid, blood glucose, liver inflammation, liver damage, fecal short-chain fatty acids (SCFAs), and gut microbiota were evaluated. It was showed that LAB supplementation prevented abnormal weight gain and liver damage induced by HFHCD, while showing different effects on the blood lipid and blood glucose regulation. Among all the strains, Lactobacillus reuteri CCFM8631 showed the highest capacity in alleviation of NAFLD. Furthermore, at the end of the treatment, the fecal SCFAs content and the abundance of Bifidobacterium, Lactobacillus, and Desulfovibrio significantly increased, whilst the abundance of Mucispirillum, Turicibacter, SMB53, and Allobaculum were significantly reduced. Correlation analysis between intestinal and liver pathological indicators showed that regulation on the SCFAs and gut microbiota was significantly associated with NAFLD alleviation. Therefore, the regulation on the SCFAs and gut microbiota by Lactobacillus reuteri CCFM8631 may be an important way for it to relieve NAFLD. This study provides a reference for the preparation of probiotic products in NAFLD prevention. This study provides a new option for the prevention and treatment of NAFLD. Also, it provides a reference for the development of probiotic preparations for NAFLD.

Cite this article

JIAO Ting , ZHU Huiyue , SI Qian , XU Mengshu , SUN Shanshan , MA Fangli , WANG Gang , ZHAO Jianxin , ZHANG Hao , CHEN Wei . Significant correlation between relieving of non-alcoholic fatty liver disease and regulation on gut microbiota and short-chain fatty acids in mice by Lactobacillus reuteri CCFM8631[J]. Food and Fermentation Industries, 2020 , 46(10) : 35 -43 . DOI: 10.13995/j.cnki.11-1802/ts.023271

References

[1] LI J, ZOU B, YEO Y H, et al. Prevalence, incidence, and outcome of non-alcoholic fatty liver disease in Asia, 1999-2019: A systematic review and meta-analysis[J]. The Lancet Gastroenterology & Hepatology, 2019, 4(5): 389-398.
[2] XIE C, YAGAI T, LUO Y, et al. Activation of intestinal hypoxia-inducible factor 2alpha during obesity contributes to hepatic steatosis[J]. Nat Med, 2017, 23(11): 1 298-1 308.
[3] WESOLOWSKI S R, KASMI K C, JONSCHER K R, et al. Developmental origins of NAFLD: A womb with a clue[J]. Nat Rev Gastroenterol Hepatol, 2017, 14(2): 81-96.
[4] 中华医学会肝病学分会脂肪肝和酒精性肝病学组, 中国医师协会脂肪性肝病专家委员会. 非酒精性脂肪性肝病防治指南(2018年更新版)[J].使用肝脏病杂志, 2018,21(2):177-186.
[5] JIANG W, WU N, WANG X, et al. Dysbiosis gut microbiota associated with inflammation and impaired mucosal immune function in intestine of humans with non-alcoholic fatty liver disease[J]. Sci Rep, 2015(5):8 096.
[6] LEUNG C, RIVERA L R, FURNESS J B, et al. The role of the gut microbiota in NAFLD[J]. Nature Reviews Gastroenterology & Hepatology, 2016,13(7):412-425.
[7] LEUNG C, RIVERA L, FURNESS J B, et al. The role of the gut microbiota in NAFLD[J]. Nat Rev Gastroenterol Hepatol, 2016, 13(7): 412-425.
[8] TILG H, CANI P D, MAYER E A. Gut microbiome and liver diseases[J]. Gut, 2016, 65(12): 2 035-2 044.
[9] MIHAILOVIC' M, ZˇIVKOVIC' M, JOVANOVIC' J A, et al. Oral administration of probiotic Lactobacillus paraplantarum BGCG11 attenuates diabetes-induced liver and kidney damage in rats[J]. Journal of Functional Foods, 2017(38):427-437.
[10] 王晓伟, 高鹏飞, 姚国强, 等. 非酒精性脂肪肝与肠道菌群及益生菌的相关性研究进展[J].现代预防医学, 2015, 42(12): 2 153-2 155;2 174.
[11] 司倩, 焦婷, 杨树荣, 等. 两歧双歧杆菌缓解Ⅱ型糖尿病的效果差异及机制分析[J].食品与发酵工业,2019,45(22):12-19.
[12] 朱广素, 王刚, 王园园, 等. 植物乳杆菌通过调节肠道短链脂肪酸水平缓解代谢综合征[J].食品科学,2019, 40(13): 102-109.
[13] BEDOSSA P, CONSORTIUM F P. Utility and appropriateness of the fatty liver inhibition of progression (FLIP) algorithm and steatosis, activity, and fibrosis (SAF) score in the evaluation of biopsies of nonalcoholic fatty liver disease[J]. Hepatology, 2014, 60(2): 565-575.
[14] WANG G, XU Q, JIN X, et al. Effects of lactobacilli with different regulatory behaviours on tight junctions in mice with dextran sodium sulphate-induced colitis[J]. Journal of Functional Foods, 2018:47:107-115.
[15] WANG L, PAN M, LI D, et al. Metagenomic insights into the effects of oligosaccharides on the microbial composition of cecal contents in constipated mice[J]. Journal of Functional Foods, 2017,38(PartA):486-496.
[16] 朱广素, 王刚, 王园园, 等. 两株具有缓解代谢综合征功能的人源益生菌的安全性评价[J].食品与发酵工业,2018, 44(8): 57-64.
[17] 张如春, 司华哲, 陈双双, 等. 罗伊氏乳杆菌在畜禽生产中应用的研究进展[J].动物营养学报,2019, 31(3): 1 031-1 036.
[18] 冯秀娟, 左芳雷, 陈丽丽, 等. 乳酸菌耐酸耐胆盐分析与胆盐水解酶研究[J].中国食品学报, 2013, 13(11): 139-147.
[19] LIN H V, FRASSETTO A, KOWALIK E J J R, 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): 35 240.
[20] GAO Z, YIN J, ZHANG J, et al. Butyrate improves insulin sensitivity and increases energy expenditure in mice[J]. Diabetes, 2009, 58(7): 1 509-1 517.
[21] ZHOU D, CHEN Y W, ZHAO Z H, et al. Sodium butyrate reduces high-fat diet-induced non-alcoholic steatohepatitis through upregulation of hepatic GLP-1R expression[J]. Exp Mol Med, 2018, 50(12): 157.
[22] 饶文婷, 罗尚菲, 张雅心, 等. 阿魏酸对高脂血症小鼠肝脂肪变性及肠道菌群的调节作用[J].中国实验动物学报,2020,28(1):36-42.
[23] DEL CHIERICO F, NOBILI V, VERNOCCHI P, et al. Gut microbiota profiling of pediatric nonalcoholic fatty liver disease and obese patients unveiled by an integrated meta-omics-based approach[J]. Hepatology, 2017, 65(2): 451-464.
[24] SHIN N-R, WHON T W, BAE J W. Proteobacteria: microbial signature of dysbiosis in gut microbiota[J]. Trends in Biotechnology, 2015, 33(9): 496-503.
[25] DIN A U, HASSAN A, ZHU Y, et al. Inhibitory effect of Bifidobacterium Bifidum ATCC 29521 on colitis and its mechanism[J]. The Journal of Nutritional Biochemistry, 2020,79: 108 353.
[26] 王佳丽, 修成奎, 杨静, 等. 人参三七川芎提取物对高糖高脂诱导血管衰老小鼠肠道菌群的影响[J/OL].中国中药杂志,1-11.https://doi.org/10.19540/j.cnki.cjcmm.20200117.401.
[27] WAN P, PENG Y, CHEN G, et al. Modulation of gut microbiota by Ilex kudingcha improves dextran sulfate sodium-induced colitis[J]. Food Research International, 2019, 126:108 595.
[28] WAN X Z, LI T T, ZHONG R T, et al. Anti-diabetic activity of PUFAs-rich extracts of Chlorella pyrenoidosa and Spirulina platensis in rats[J]. Food and Chemical Toxicology, 2019, 128:233-239.
[29] HUANG K, YU W, LI S, et al. Effect of embryo-remaining oat rice on the lipid profile and intestinal microbiota in high-fat diet fed rats[J]. Food Research International, 2020, 129:108 816.
[30] MASANORI H, TAKAMASA M, SATOMI H, et al. Comparative analysis of the intestinal flora in type 2 diabetes and nondiabetic mice[J].Experimental animals, 2017, 66(4):405-416.
[31] ZHU W, GREGORY J C, ORG E, et al. Gut microbial metabolite TMAO enhances platelet hyperreactivity and thrombosis risk[J]. Cell, 2016, 165(1): 111-124.
[32] TAN X, LIU Y, LONG J, et al. Trimethylamine N-oxide aggravates liver steatosis through modulation of bile acid metabolism and inhibition of farnesoid X receptor signaling in nonalcoholic fatty liver disease[J]. Molecular Nutrition & Food Research, 2019, 63(17): 1 900 257.
[33] 程俊俊, 吴霞. 肠道微生物代谢产物氧化三甲胺与非酒精性脂肪性肝病研究进展[J]. 肝脏, 2017, 22(11): 1 056-1 058.
[34] 张丹琴, 杨帆, 李胜保. 非酒精性脂肪性肝病患者血清TLR4、IL-10、 IL-22与肠道菌群的相关性[J]. 肝脏, 2019, 24(12): 1 432-1 434.
[35] 陈新君. 复方四君子汤及党参多糖调节溃疡性结肠炎小鼠肠道菌群的作用研究[D]. 兰州:兰州大学, 2016.
[36] 刘保文. 肝硬化及肝硬化合并糖尿病患者肠道微生态研究[D]. 天津:天津医科大学, 2017.
[37] 李帆. 中国人群非酒精性脂肪性肝病患者肠道菌群结构的研究[D]. 北京:中国人民解放军医学院, 2014.
Outlines

/