Abstract
Sustained consumption of dietary fats induces endothelial dysfunction and insulin resistance in experimental models and humans. Endothelial dysfunction, manifested by reduced endothelium-dependent dilation, is a hallmark of several cardiovascular diseases and obesity. Indeed, exercise training and caloric restriction attenuate endothelial dysfunction and delay the onset or reduce the magnitude of vascular diseases and insulin resistance. Article, see p 1176 A major pathway controlling endothelium-dependent vasodilation is via endothelial NO synthase (eNOS) generation of the vasodilatory, anti-inflammatory, antioxidant autacoid, NO. NO can serve as a paracrine mediator promoting various beneficial functions through several mechanisms including activation of soluble guanylyl cyclase and nitrosation of cellular proteins and lipids that promote vascular relaxation and attenuate proinflammatory pathways. In this issue of Circulation Research , Sansbury et al1 provide striking evidence that eNOS-derived NO actively participates in regulating the extent of adiposity. Previous work has …
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