title: Lactobacillus casei Shirota protects from fructose-induced liver steatosis: a mouse model.
abstract: 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)-γ 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.
authors: Department of Nutritional Medicine-180 a, University of Hohenheim, Fruwirthstrasse 12, 70599 Stuttgart, Germany.
authors: Sabine
authors: S
authors: Wagnerberger
authors: Astrid
authors: A
authors: Spruss
authors: Giridhar
authors: G
authors: Kanuri
authors: Carolin
authors: C
authors: Stahl
authors: Markus
authors: M
authors: Schröder
authors: Walter
authors: W
authors: Vetter
authors: Stephan C
authors: SC
authors: Bischoff
authors: Ina
authors: I
authors: Bergheim
mesh_terms: D000410:Alanine Transaminase / Q000032:analysis / Q000378:metabolism; D000818:Animals; D002087:Butyrates / Q000097:blood; D002460:Cell Line; D049109:Cell Proliferation; D002839:Chromans / Q000819:agonists / Q000494:pharmacology; D016172:DNA Fingerprinting; D004269:DNA, Bacterial / Q000235:genetics / Q000302:isolation & purification*; D004195:Disease Models, Animal; D005234:Fatty Liver / Q000139:chemically induced / Q000473:pathology* / Q000517:prevention & control*; D005632:Fructose / Q000009:adverse effects*; D007004:Hypoglycemic Agents / Q000819:agonists / Q000494:pharmacology; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000187:drug effects; D007780:Lacticaseibacillus casei / Q000235:genetics / Q000378:metabolism*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D065626:Non-alcoholic Fatty Liver Disease; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism; D017422:Sequence Analysis, DNA; D015398:Signal Transduction; D045162:Thiazolidinediones / Q000819:agonists / Q000494:pharmacology; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism; D000077288:Troglitazone; D015854:Up-Regulation
chemical_list: D002087:Butyrates; D002839:Chromans; D004269:DNA, Bacterial; D007004:Hypoglycemic Agents; D047495:PPAR gamma; D045162:Thiazolidinediones; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; D005632:Fructose; D000410:Alanine Transaminase; D000077288:Troglitazone