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Fig. 6 | Cardiovascular Diabetology

Fig. 6

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

Fig. 6

Effects of nitric oxide (NO) donor on skeletal muscle insulin signaling in wild-type (WT) mice (Group 1A). Western blotting was performed for plantaris muscle extract for phosphorylation (p) of Akt at Ser473 and Thr308 (a, c) and for glycogen synthase kinase (GSK) 3β phosphorylation at Ser9 residue (b, d). Chemiluminescence on 4–12 % SDS-PAGE gels was quantified for skeletal muscle. Insulin-induced protein phosphorylation was quantified as the ratio phosphorylation and total Akt or GSK chemiluminescence in skeletal muscle extract after a 2 h hyperinsulinemic-euglycemic clamp. β-actin was used as a loading control. Data are arbitrary units (AU) expressed as mean ± SEM (n = 7). *p < 0.05 by two-way ANOVA. NS not significant (p ≥ 0.05)

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