Metabolic Endotoxemia Initiates Obesity and Insulin Resistance

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FIG. 7.
FIG. 7.

CD14 mutant mice resist high-fat diet–induced glucose intolerance, inflammation, and increased visceral fat mass. A: Plasma glucose (mmol/l) following an intraperitoneal glucose load (1 g/kg) in WT mice fed a normal diet (WT-CT; n = 6) (▪) or a high-fat diet (WT-HF; n = 6) (▴) for 4 weeks and CD14 mutant mice fed a normal diet (CD14-CT; n = 5) (•) or fed a high-fat diet (CD14-HF; n = 5) (□). The inset represents the area under curve of the same groups. B: Plasma insulin concentration (pmol/l) 30 min before (−30) and 30 min after (30) intraperitoneal glucose administration in WT-CT (n = 6) (□), WT-HF (n = 6) (▪), CD14-CT (n = 5) ( ▒), and CD14-HF (n = 5) (Graphic) mice. C: Visceral and subcutaneous adipose tissue weight (percent of body weight) in WT-CT (n = 6) (□), WT-HF (n = 6) (▪), CD14-CT (n = 5) (▒), and CD14-HF (n = 5) (Graphic) mice. Adipose tissue (D) and liver (E) mRNA concentrations of TNF-α, IL-1, IL-6, and PAI-1 in WT-CT (n = 6) (□), WT-HF (n = 6) (▪), CD14-CT (n = 5) (▒), and CD14-HF (n = 5) (Graphic) mice. Data are means ± SE. Data with different superscript letters are significantly different at P < 0.05, according to the post hoc ANOVA statistical analysis.

This Article

  1. Diabetes vol. 56 no. 7 1761-1772