Lactobacillus casei Shirota protects from fructose-induced liver steatosis: A mouse model

Lactobacillus casei Shirota protects from fructose-induced liver steatosis: A mouse model
复制标题

DOI:
10.1016/j.jnutbio.2012.01.014
复制
发表时间:
2013-03-01
影响因子:
5.6
通讯作者:
Bergheim, Ina
Bergheim, Ina
中科院分区:
医学2区
文献类型:
--
作者:
Wagnerberger, Sabine;Spruss, Astrid;Bergheim, Ina

文献摘要

被引文献

相似文献

为了检验干酪乳杆菌Shirota(Lcs)在果糖诱导的脂肪变性的小鼠模型中防止非酒精性脂肪性肝病(NAFLD)发作的假设,C57 BL/6 J小鼠喂食自来水或30%果糖溶液+/- Lcs 8周。长期摄入30%果糖溶液导致肝脂肪变性和血浆丙氨酸氨基转移酶(ALT)水平显著增加,而Lcs治疗可使其减弱。发现在十二指肠中的两个果糖处理组中紧密连接蛋白occludin的蛋白质水平显著较低,而肠的这一部分中的微生物群组成不受影响。Lcs处理显著减弱了仅用果糖处理的小鼠肝脏中发现的Toll样受体(TLR)4信号级联的激活。此外,在用Lcs过氧化物酶体增殖物激活受体(PPAR)-γ活性处理的果糖喂养小鼠的肝脏中,明显高于仅喂养果糖的小鼠。总之,本研究的结果表明,膳食摄入Lcs通过涉及肝脏TLR-4信号级联衰减的机制来防止果糖诱导的NAFLD的发作。(C)2013 Elsevier Inc. All rights reserved.
To test the hypothesis that Lactobacillus casei Shirota (Lcs) protects against the onset of non-alcoholic fatty liver disease (NAFLD) in a mouse model of fructose-induced steatosis, C57BL/6J mice were either fed tap water or 30% fructose solution +/- Lcs for 8 weeks. Chronic consumption of 30% fructose solution led to a significant increase in hepatic steatosis as well as plasma alanine-aminotransferase (ALT) levels, which was attenuated by treatment with Lcs. Protein levels of the tight junction protein occludin were found to be markedly lower in both fructose treated groups in the duodenum, whereas microbiota composition in this part of the intestine was not affected. Lcs treatment markedly attenuated the activation of the Toll-like receptor (TLR) 4 signalling cascade found in the livers of mice only treated with fructose. Moreover, in livers of fructose fed mice treated with Lcs peroxisome proliferator-activated receptor (PPAR)-gamma activity was markedly higher than in mice only fed fructose. Taken together, the results of the present study suggest that the dietary intake of Lcs protects against the onset of fructose-induced NAFLD through mechanisms involving an attenuation of the TLR-4-signalling cascade in the liver. (C) 2013 Elsevier Inc. All rights reserved.