Conclusion
ADF exerts metabolic and endothelial protective benefits. The improvement of endothelial function was partly mediated by increased adiponectin, representing an important mechanism for the beneficial vascular effects resulting from ADF.
Methods
Control mice (m Lepr db ) and diabetic mice (Leprdb ) were treated with 12-weeks of ADF. Glucose metabolism, endothelial function, and adipokine profile were assessed.
Objective
We aimed to test the hypothesis that ADF protects against diabetes-associated endothelial dysfunction, at least partly through modulating adipokine profiles.
Results
ADF reduced fasting blood glucose level and homeostatic model assessment for insulin resistance (HOMA-IR), and improved insulin sensitivity. ADF improved endothelium-dependent vasorelaxation of small mesenteric arteries (SMA) of Leprdb mice. The improvement in endothelial function was largely attenuated by incubation with the nitric oxide synthase inhibitor, L-NAME. These ADF-induced metabolic and vascular benefits were accompanied by increased circulating adiponectin. Adenovirus-mediated adiponectin supplementation improved endothelial function in Leprdb mice, supporting endothelial protective roles in diabetes-associated endothelial dysfunction. Protein tyrosine nitration is a post-translational modification that serves as a marker of oxidative stress. Nitrotyrosine protein levels in SMA and mesenteric adipose tissue (MAT) were elevated in Leprdb mice. ADF reduced nitrotyrosine protein in SMA, but not in MAT, of Leprdb mice.