Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 8, 2013
Publication Date: March 13, 2013
Repository URL: http://handle.nal.usda.gov/10113/56736
Citation: Zeng, H., Liu, J., Jackson, M.I., Zhao, F., Yan, L., Combs, G.F. 2013. Fatty liver accompanies an increase in Lactobacillus species in the hind gut of C57BL/6 mice fed a high-fat diet. Journal of Nutrition. doi:10.3945/jn.112.172460. Interpretive Summary: Obesity has been linked to the development of nonalcoholic fatty liver disease (NAFLD). As the liver receives approximately 70% of its blood supply from the intestine, and gut microbiota plays a key role in maintenance of gut-liver axis health, several lines of evidence suggest an interaction between gut microbiota and liver but the research in this area remains largely unexplored. The aim of this study is to determine the correlation of fatty liver and numerically predominant gut bacteria in a diet-induced obesity mouse model. In this study, we found that body weight and body fat percentage were significantly increased, and fatty liver phenotype occurs in C57BL/6 mice fed a high fat diet when compared with that of control group. Interestingly, we also find that fatty liver phenotype accompanies an marked increase of Lactobacillus acidophilus gut bacteria which may promote the inflammatory process. Taken together, the body fat/obesity and an increase in gut L. acidophilus bacteria may promote inflammatory process and hepatic steatitis in these mice. The information will be useful information for scientists and health-care professionals who are interested in obesity related NAFLD prevention.
Technical Abstract: High-fat diets can produce obesity and have been linked to the development of nonalcoholic fatty liver disease (NAFLD). They have also been shown to induce changes in the gut microbiome, metabolic products of which have also been linked to NAFLD. This study tested the hypothesis that high-fat feeding increases certain dominant hind gut bacteria in a C57BL/6 mouse model of obesity. We found that a high-fat diet produced significant increases in both body weight and body fat percentage in C57BL/6 mice compared with a control group fed a low-fat diet. These changes were associated with dramatic increases in lipid droplet, inflammatory cell infiltration and inducible nitric oxide synthase (iNOS) activity in the livers of mice fed the high-fat diet. Consistent with the fatty liver phenotype, plasma leptin and tumor necrosis factor (TNF'' levels were elevated in mice fed the high-fat diet, indicative of chronic inflammation. Eight out of twelve bacterial species that typically predominate hind gut microbial ecology were detected in fecal samples by DNA analysis. The DNA amount of one of these species, L. acidophilus, was 6900-fold greater in high-fat fed mice compared to controls. L. acidophilus can promote inflammatory production of cytokines such as TNF which was also elevated in high-fat fed mice. These results suggest that changes in the hindgut microbiome which accompany high fat feeding may contribute to the development of hepatic steatitis in obese mice.