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

(Downloading may take up to 30 seconds. If the slide opens in your browser, select File -> Save As to save it.)

Click on image to view larger version.

FIG. 2.
FIG. 2.

Inhibiting de novo ceramide accumulation in vivo normalizes endothelial dysfunction and hypertension in C57Bl/6 mice with diet-induced obesity. Systolic (A), mean (B), and diastolic (C) arterial blood pressure during light and dark cycles. Data are averaged from 4- × 24-h periods for 10 CON-V, 10 HF-V, 9 CON-M, and 9 HF-M mice. D: EDR. E: EIR. F: NR-mediated vasocontraction. G: Receptor (R)-mediated vasocontraction. Data are from two femoral artery segments from 18 CON-V, 23 HF-V, 15 CON-M, and 17 HF-M mice. AH: *P < 0.05 HF-V vs. all. G: #P < 0.05 HF-M vs. all. Results represent mean ± SEM. H: Representative immunoblot and densitometry of the ratio of p-eNOS at serine (S)1177 to total eNOS from aorta/iliac arterial homogenates from 8 CON-V, 13 HF-V, 6 CON-M, and 8 HF-M mice. *P < 0.05 HF-V vs. all. V, vehicle; M, myriocin.

This Article

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