Figure 3.
Supplementation with 3,3-dimethyl-1-butanol (DMB) mitigates Western-style diet (WD)-induced endothelial dysfunction. In young mice fed either a standard chow (SC) or WD and given either normal drinking water (control; SC-C, WD-C) or water supplemented with 1% DMB (3,3-dimethyl-1-butanol; SC-DMB, WD-DMB) for 8–10 wk: ex vivo carotid artery endothelium-dependent dilation (EDD) to acetylcholine (ACh) in the absence (ACh alone) or presence of the nitric oxide (NO) synthase inhibitor l-NAME (A); peak EDD to ACh alone (highest diameter achieved during the dose response) (B); ex vivo carotid artery endothelium-independent dilation to sodium nitroprusside (C); and peak carotid artery EDD to ACh in the presence of the superoxide dismutase mimetic TEMPOL (D). n = 11–13 mice/group. Data are means ± SE. *P < 0.05 SC-C vs. SC-DMB; †P < 0.05 WD-C vs. WD-DMB. Stats are two-way mixed (group × dose) ANOVA with Tukey’s post hoc test (A and C), two-way (diet × treatment) ANOVA with Šidák’s multiple comparisons tests (B), or Student’s unpaired t test (D). TEMPOL, 4-hydroxy-2,2,6,6,-tetramethylpiperidin-1-oxyl.