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Fig 1.

HFD increased body weight gain in female CD-1 mice.

(A) Growth curve of mice on HFD or chow. (B) Representative images of mice (bar length = 1 cm). (C) Energy intake. Values in (A) and (C) represent average ± SD (n = 10). * P < 0.05 compared with mice on chow, ** P < 0.01 compared with mice on chow.

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Fig 1 Expand

Fig 2.

HFD caused hypertrophy of white adipocytes.

(A) Lean mass (n = 10). (B) Fat mass (n = 10). (C) Representative images of WAT histological examinations (bar length = 100 μm). (D) Adipocyte diameter (n = 4). Values in (A), (B) and (D) represent average ± SD. ** P < 0.01 compared with mice on chow.

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Fig 2 Expand

Fig 3.

Gene expression analysis in WAT.

(A) Expression level of F4/80. (B) Expression level of Cd11b. (C) Expression level of Cd11c. (D) Expression level of Mcp-1. (E) Expression level of Tnf-α. (F) Expression level of Leptin. Values represent average ± SD (n = 4). ** P < 0.01 compared with mice on chow.

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Fig 3 Expand

Fig 4.

HFD caused whitening of BAT without significantly changing blood clearance of triglyceride.

(A) Representative images of BAT histological examinations. (B) Measurement of BAT nuclei. (C) Determination of Blood triglyceride. (D) Representative image of lipoprotein electrophoresis (C for chow and H for HFD). Values in (B) and (C) represent average ± SD (n = 4). ** P < 0.01 compared with mice on chow.

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Fig 4 Expand

Fig 5.

HFD induced hepatic steatosis.

(A) Representative images of liver histological examinations. (B) Liver triglyceride determination. (C) Blood aspartate aminotransferase. (D) Blood alanine aminotransferase. Values in (B), (C) and (D) represent average ± SD (n = 4). ** P < 0.01 compared with mice on chow.

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Fig 5 Expand

Fig 6.

Gene expression in liver.

(A) Expression level of Ppar-γ2. (B) Expression level of Cd36. (C) Expression level of Mgat1. (D) Expression level of Fgf21. Values represent average ± SD (n = 4). * P < 0.05 compared with mice on chow, ** P < 0.01 compared with mice on chow.

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Fig 6 Expand

Fig 7.

HFD impaired glucose homeostasis, which subsequently gave rise to hyperinsulinemia and pancreatic islet hypertrophy.

(A) Profiles of blood glucose concentration as function of time upon intraperitoneal injection of glucose (n = 5). (B) Profiles of glucose concentration (percentage of initial value) as a function of time upon intraperitoneal injection of insulin (n = 5). (C) Blood insulin (n = 4). (D) Representative images of pancreas histological examinations. Values in (A), (B) and (C) represent average ± SD. * P < 0.05 compared with mice on chow, ** P < 0.01 compared with mice on chow.

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Fig 7 Expand