Ceramide Mediates Vascular Dysfunction in Diet-Induced Obesity by PP2A-Mediated Dephosphorylation of the eNOS-Akt Complex

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FIG. 3.
FIG. 3.

Arterial function in fat-fed mice with targeted disruption of des1. des1+/− and des1+/+ mice were placed on CON or HF diets for 3 months. Vascular ceramide content (A), body composition (B), and AUC during a glucose tolerance test (GTT) (C) in 9 HF des1+/+, 11 HF des1+/−, 12 CON des1+/+, and 13 CON des1+/− mice. Fasting (6 h) blood glucose (mg/dL) before the GTT in panel C was higher in HF (164 ± 10) vs. CON des1+/+ (122 ± 11) mice and HF (182 ± 11) vs. CON des1+/− (147 ± 9) animals. D and E: EDR and NR-mediated vasocontraction from HF vs. CON des1+/+ mice. F and G: EDR and NR-mediated vasocontraction from HF vs. CON des1+/− mice. H: EIR from all groups. Data are from two femoral artery segments from each of the des1+/+ and des1+/− mice. I: Representative immunoblot and densitometry of the ratio of p-eNOS Ser1177 to total eNOS from aorta/iliac arterial homogenates from des1+/+ and des1+/− mice. *P < 0.05 CON vs. HF; #P < 0.05 des1+/+ vs. des1+/−. Results represent mean ± SEM. AU, arbitrary unit.

This Article

  1. Diabetes vol. 61 no. 7 1848-1859