A high-fat diet (HFD) is one of the causes of hepatic steatosis. We previously demonstrated that Enterococcus faecalis FK-23 (FK-23), a type of lactic acid bacteria, exhibits an anti-obesity effect in mice fed a HFD. In the present study, we examined the effects of FK-23 on HFDinduced hepatic steatosis. Male C57BL/6 mice were divided into four groups and given one of four treatments: standard diet (SD); standard diet supplemented with FK-23 (SD þ FK); HFD; or HFD supplemented with FK-23 (HFD þ FK). For the administration of FK-23, the drinking water was supplemented with FK-23 at a concentration of 2 % (w/w). After 11 weeks, histological findings revealed hepatic steatosis in the liver of HFD-fed mice; however, this effect was attenuated by the administration of FK-23. The expression levels of genes involved in fatty acid oxidation in the liver tissue were significantly reduced in the HFD group compared with the SD group, but FK-23 supplementation tended to up-regulate the expression levels of these genes. Our findings show that the inhibitory effect of FK-23 against hepatic steatosis in HFD-fed mice can be explained by the prevention of fat accumulation in the liver through the modulation of the activities of genes involved in hepatic fatty acid oxidation.

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Faecalibacterium prausnitzii is one of the most abundant bacteria in the human gut microbiota. This bacterium is reported to serve an important role in inflammatory bowel diseases. In the present study, the preventive effects of F. prausnitzii on a dextran sodium sulfate (dSS)-induced colitis model in mice were investigated. BalB/c mice were fed with 5% dSS in drinking water. administration of live or inactivated F. prausnitzii was initiated 7 days prior to the start of DSS feeding. Mucosal cytokines were analyzed by reverse transcription-quantitative PCR. Histological analysis of colon mucosa was also performed. The symptoms of DSS-induced colitis (weight loss, diarrhea, bloody stools and colon shortening) were significantly improved in the group administered live F. prausnitzii, but not in the other groups. There were no significant differences in the expression of proinflammatory cytokines; however, the expression of mucosal cytokines appeared to be markedly reduced in the live F. prausnitzii-administered group compared with the dSS-fed control. The results suggested that preventive administration of 'live', but not inactivated, F. prausnitzii protected the colon against dSS-induced colitis. live F. prausnitzii were also administered therapeutically following the induction of colitis, resulting in an improved histological score in mice.

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