Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract only
Publication Acceptance Date: 11/2/2012
Publication Date: 4/9/2013
Citation: Zeng, H., Liu, J., Jackson, M.I., Yan, L., Combs, G.F. 2013. Fatty liver accompanies an increase of Lactobacillus acidophilus in the hind gut of C57/BL mice fed a high-fat diet. Federation of American Societies for Experimental Biology Conference. 27:1067.4. Interpretive Summary:
Technical Abstract: High-fat diets can produce obesity and have been linked to the development of nonalcoholic fatty liver disease (NAFLD), which also induces changes in the gut microbiome. This study tested the hypothesis that high-fat feeding increases certain predominate 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-alpha) 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-alpha'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 steatohepatitis in obese mice.