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Fig. 7 | Cardiovascular Diabetology

Fig. 7

From: Tissue inflammation and nitric oxide-mediated alterations in cardiovascular function are major determinants of endotoxin-induced insulin resistance

Fig. 7

Mean arterial blood pressure (MAP in mmHg, Panel a), blood glucose (in mg/dL, Panel b), and glucose infusion rate (GIR in mg · kg−1 · min−1, Panel c), for saline-treated (SAL) or lipopolysaccharide (LPS)-treated iNOS+/+ (WT) or iNOS−/− (KO) mice during a hyperinsulinemic-euglycemic clamp (Group 2A). Mice were treated with LPS (2 μg/g BW) 4 h prior to clamp onset (t = 0 min). Glucose (50 %) was infused to maintain euglycemia at 120 mg/dL during steady state (t = 80–120 min). Insulin sensitivity was represented as whole-body Rg (mg · kg−1 · min−1) vs. plasma insulin level (ng/ml) for basal and clamp time periods in iNOS+/+ (d) and iNOS−/− mice (e). Basal glucose uptake values were determined from plasma samples at −10 min and 0 min before the onset of the clamp. Steady state (clamp) levels were determined from plasma samples at 80, 90, 100, and 120 min. MAP (a) was summarized as mean during end of the clamp (t = 60–120 min). Data are expressed as mean ± SEM (n = 7–8). *p < 0.05 vs. WT + SAL compared by repeated measures two-way ANOVA for MAP (30–120 min) and GIR (80–120 min)

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