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Fig 1.

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Fig 2.

Effects of a high-fat diet on body weight and metabolism of glucolipids in obese mice.

(A) Changes in body weight over 12 weeks; (B) Changes in relative body weight gain in mice; (C) Epididymal adiposity index; (D) Perirenal adipose tissue; (E) Glucose tolerance test (GTT); (F) Serum NEFA. A and B, n = 10 each group; C and D, n = 4 each group; E,n = 5 each group; F,n = 9–10 each group.**P < 0.01, ***P < 0.001,****P < 0.0001 vs Control group.

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Fig 3.

Renal changes in obese mice induced by high-fat diet obesity mice.

(A) The content of kidney total cholesterol (TCH) and (B) kidney triglyceride (TG), **P < 0.01 versus Control group, n = 5 each group. (C) Sections of kidney tissue stained with PAS, magnification, 400×, and (D) The percentage of renal tissue stained with PAS, *P < 0.05 versus Control group, n = 3 each group. (E) Transmission electron microscopy of renal ultramicrostructure, magnification, 25000×, n = 3 each group. (F) Malondialdehyde (MDA) content, superoxide dismutase(SOD)activity, catalase (CAT) activity, *P < 0.05, **P < 0.01, n = 3–4 each group.

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Fig 4.

Changes in metabolomics of renal tissue in high-fat diet obesity mice.

(A) Both groups identified different types and quantities of metabolic compounds. Positive and negative ion volcano plots (B, C), the blue and red round dots indicate metabolites that are downregulated and upregulated. (D) Positive and (E) negative ion partial least squares discrimination analysis (PLS-DA) permutation test. (F) The hierarchy of clustering of differential metabolites in negative ion modes. A-F, n = 6 each group.

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Fig 5.

Transcriptomic changes of kidney in obese mice induced by high-fat diet.

(A) Principal Component Analysis (PCA). (B) The number of different genes between the two groups. (C) Volcanic map of differential gene expression distribution. (D) Heat map of correlation coefficient between two groups of mouse kidney samples. A-D, n = 3 each group.

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Fig 6.

GO enrichment pathway and FPKM of differential genes expression.

(A) GO enrichment pathways of upregulated differential genes (B)The FPKM of Ugt1a9 gene. (C) The FPKM of Ugt2b1 gene. (D) The FPKM of Ugt2b36 gene. A-E, **P < 0.01, n = 3 each group.

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Table 1.

Transcriptomic analysis metabolism-related pathways by KEGG enrichment.

(Obesity vs Control).

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Fig 7.

Network analysis of differential metabolites and genes ascorbate and aldarate metabolism pathway.

Parallelogram represents differential genes, rectangle represents differential metabolites, green means down-regulated, red means up-regulated.

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Fig 8.

The metabolic characteristics and key biological pathways of kidney injury induced by high-fat diet in obese mice.

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