Hence, the protective mechanism of dietary DMG on development of pulmonary hypertension can, at least partly, be attributed to its effect on fat metabolism. Further, Sarafadis and Bakris
(2007) attribute an increase in oxidative stress, next to increased arterial stiffness and vasoconstriction, and decreased endothelium-dependent vasodilation, being associated with an increase in plasma NEFA level. In addition, in vivo data of Sainsbury et al. (2004) presume oxidative stress to be at the basis of the detrimental effect of increased NEFA level on endothelial dysfunction. Concordantly, the observed effect of DMG on NEFA suggests an indirect
antioxidant effect of DMG.
Hence, the protective mechanism of dietary DMG on development of pulmonary hypertension can, at least partly, be attributed to its effect on fat metabolism. Further, Sarafadis and Bakris(2007) attribute an increase in oxidative stress, next to increased arterial stiffness and vasoconstriction, and decreased endothelium-dependent vasodilation, being associated with an increase in plasma NEFA level. In addition, in vivo data of Sainsbury et al. (2004) presume oxidative stress to be at the basis of the detrimental effect of increased NEFA level on endothelial dysfunction. Concordantly, the observed effect of DMG on NEFA suggests an indirectantioxidant effect of DMG.
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