Lactobacillus casei strain Shirota protects against nonalcoholic steatohepatitis development in a rodent model

Am J Physiol Gastrointest Liver Physiol. 2013 Dec;305(12):G911-8. doi: 10.1152/ajpgi.00225.2013. Epub 2013 Oct 10.


Gut microbiota alterations are associated with various disorders. In this study, gut microbiota changes were investigated in a methionine-choline-deficient (MCD) diet-induced nonalcoholic steatohepatitis (NASH) rodent model, and the effects of administering Lactobacillus casei strain Shirota (LcS) on the development of NASH were also investigated. Mice were divided into three groups, given the normal chow diet (NCD), MCD diet, or the MCD diet plus daily oral administration of LcS for 6 wk. Gut microbiota analyses for the three groups revealed that lactic acid bacteria such as Bifidobacterium and Lactobacillus in feces were markedly reduced by the MCD diet. Interestingly, oral administration of LcS to MCD diet-fed mice increased not only the L. casei subgroup but also other lactic acid bacteria. Subsequently, NASH development was evaluated based on hepatic histochemical findings, serum parameters, and various mRNA and/or protein expression levels. LcS intervention markedly suppressed MCD-diet-induced NASH development, with reduced serum lipopolysaccharide concentrations, suppression of inflammation and fibrosis in the liver, and reduced colon inflammation. Therefore, reduced populations of lactic acid bacteria in the colon may be involved in the pathogenesis of MCD diet-induced NASH, suggesting normalization of gut microbiota to be effective for treating NASH.

Keywords: Lactobacillus casei strain shirota; gut microbiota; inflammation; lipid metabolism; nonalcoholic steatohepatitis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bifidobacterium / isolation & purification
  • Bifidobacterium / metabolism
  • Choline Deficiency / metabolism
  • Disease Models, Animal
  • Fatty Liver* / metabolism
  • Fatty Liver* / pathology
  • Fatty Liver* / prevention & control
  • Gastrointestinal Tract* / metabolism
  • Gastrointestinal Tract* / microbiology
  • Gene Expression Profiling / methods
  • Inflammation / metabolism
  • Inflammation / pathology
  • Lacticaseibacillus casei / metabolism*
  • Lipid Metabolism
  • Liver / metabolism
  • Liver / pathology
  • Methionine / deficiency
  • Methionine / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Microbiota / physiology*
  • Non-alcoholic Fatty Liver Disease


  • Methionine