Fig 1.
(A) Representative photographs of sections of hamster kidneys stained by H&E and for expression of kidney injury molecule-1 (KIM-1) and high-mobility group box 1 protein (HMGB1), (B) serum creatinine levels and percentages of (C) KIM-1- and (D) HMGB1-positive cells. The extent of injury in these kidneys was evaluated after 8 months on experimental diets including the normal group (n = 6), monosodium glutamate-treated group (MSG, n = 6), high-fat and high-fructose diet-treated group (HFF, n = 6) and the MSG and HFF diet-treated group (MSG+HFF, n = 6). Findings are presented as mean ± SEM. *, **, *** are p < 0.05, p < 0.01 and p < 0.0001, respectively, compared with normal control or MSG or HFF.
Fig 2.
Fecal microbial composition in hamsters at different taxonomic levels.
The columns represent a normal group (n = 10), monosodium glutamate-treated group (MSG) (n = 10), high-fat and high-fructose diet-treated (HFF) (n = 10) and MSG and HFF diet-treated (MSG+HFF) (n = 10).
Fig 3.
Composition of the gut microbiota.
Heat map of the top 35 bacterial genera identified from hamster fecal DNA. The abundances were arranged using unsupervised hierarchical cluster analysis (blue, low abundance; red, high abundance).
Fig 4.
Alpha diversity of the sequence reads from DNA extracted from hamster feces for each group.
(A) rarefaction analysis of the observed taxa and (B) the Shannon index. (C) Beta diversity, UPMGA clustering trees-weighted Unifrac distance. The results of clustering using two distance matrixes were combined with the overall percentages of relative abundance among all samples at phylum level.
Table 1.
Pairwise comparisons of differentially produced urine metabolites among experimental groups.
Fig 5.
Postulated mechanism by which the MSG+HFF diet might cause kidney injury.