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

  • 2013-03
  • The Journal of Nutritional Biochemistry 24(3)
    • S. Wagnerberger
    • Astrid Spruss
    • Giridhar Kanuri
    • Carolin Stahl
    • M. Schröder
    • W. Vetter
    • S. Bischoff
    • I. Bergheim

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.

Research Insights

SupplementHealth OutcomeEffect TypeEffect Size
Lactobacillus casei Lc-11Increased PPAR-γ ActivityBeneficial
Moderate
Lactobacillus casei Lc-11Reduced Hepatic SteatosisBeneficial
Large
Lactobacillus casei Lc-11Reduced TLR-4 Signalling ActivityBeneficial
Moderate
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