Table 1.
Primers used for mRNA detection.
Table 2.
Nutritional and weight parameters.
Figure 1.
Lactobacillus rhamnosus GG ameliorates fructose-induced hepatic fatty acid accumulation.
Representative Oil-Red-O (A) and hematoxilin & eosin (B) stainings showing fat accumulation in the liver. Abbreviations: C, control diet; F, high-fructose diet; CLGG, control diet with Lactobacillus rhamnosus GG (LGG) supplementation; FLGG, F with LGG supplementation.
Figure 2.
Lactobacillus rhamnosus GG modulates fructose-induced hepatic fatty acid metabolism.
Hepatic ChREBP (A), ACC1 (B) and FAS (C) mRNA expression was measured. Concentrations of triglycerides in the liver were analysed (D). Data are shown as means ± SEM (**P<0.01; ***P<0.001; n = 4–6). Abbreviations: see Figure 1; ChREBP, carbohydrate response element-binding protein; ACC1, acetyl-CoA carboxylase 1; FAS, fatty acid synthase.
Figure 3.
Lactobacillus rhamnosus GG ameliorates fructose-induced liver inflammation.
Hepatic TNF-α (A), IL-1β (B) and IL-8R (C) mRNA expression was measured. Data are shown as means ± SEM (*P<0.05; n = 4–6). Abbreviations: see Figure 1; TNF-α, tumor necorsis factor alpha; IL-1β, interleukin 1 beta; IL-8R, interleukin 8 receptor.
Figure 4.
Lactobacillus rhamnosus GG improves markers of intestinal barrier function.
The tight junction molecules occludin (A), and claudin-1 (B), as well as the inflammatory marker pIκB kinase (C) were analysed in the proximal intestine. Representative western blots and quantitative analyses of the blots are shown (A–C). LPS in portal plasma was measured (D). Data are shown as means ± SEM (*P<0.05, **P<0.01; n = 4–6). Abbreviations: see Figure 1; LPS; lipopolysaccharides.
Figure 5.
Lactobacillus rhamnosus GG elevates bacterial numbers in the distal small intestine.
Total bacterial numbers (A), LGG numbers (B), the phyla Firmicutes (C), and Bacteriodetes (D) were measured via qPCR. Data are shown as means ± SEM (**P<0.01, ***P<0.001; n = 5–6). Abbreviations: see Figure 1.
Figure 6.
Lactobacillus rhamnosus GG improves diet-induced NAFLD.
LGG ameliorates high-fructose diet-induced NAFLD via modulation of the intestinal microbiota. LGG products e.g. lactate may increase butyrate producing Firmicutes leading to an improved intestinal barrier and reduced portal plasma LPS concentrations as well as a decreased inflammation and fatty acid accumulation in the liver. Abbreviations: NAFLD, non-alcoholic fatty liver disease; LPS, lipopolysaccharides.