Abstract
Our objective was to determine whether the endothelial nitric oxide synthase (eNOS) Glu298Asp polymorphism influences vascular response to raised NEFA enriched with saturated fatty acids (SFA) or long-chain (LC) n-3 polyunsaturated fatty acids (PUFA). Subjects were prospectively recruited for genotype (Glu298, n = 30 and Asp298, n = 29; balanced for age and gender) consumed SFA on two occasions, with and without the substitution of 0.07 g fat/kg body weight with LC n-3 PUFA, and with heparin infusion to elevate NEFA. Endothelial function was measured before and after NEFA elevation (240 min), with blood samples taken every 30 min. Flow-mediated dilation (FMD) decreased following SFA alone and increased following SFA+LC n-3 PUFA. There were 2-fold differences in the change in FMD response to the different fat loads between the Asp298 and Glu298 genotypes (P = 0.002) and between genders (P < 0.02). Sodium nitroprusside-induced reactivity, measured by laser Doppler imaging with iontophoresis, was significantly greater with SFA+LC n-3 PUFA in all female subjects (P < 0.001) but not in males. Elevated NEFA influences both endothelial-dependent and endothelial-independent vasodilation during the postprandial phase. Effects of fat composition appear to be genotype and gender dependent, with the greatest difference in vasodilatory response to the two fat loads seen in the Asp298 females.
Highlights
Our objective was to determine whether the endothelial nitric oxide synthase Glu298Asp polymorphism influences vascular response to raised nonesterified fatty acids (NEFA) enriched with saturated fatty acids (SFA) or long-chain (LC) n-3 polyunsaturated fatty acids (PUFA)
The key component in the regulation of vascular homeostasis is nitric oxide (NO), a potent vasodilator produced by endothelial nitric oxide synthase.While a number of mechanisms may be responsible for mediating dietary effects, the final common pathway appears to be via fatty acid-dependent alterations in either the production or stability of NO, or the action of NO on the smooth muscle layer [8, 12,13,14], with eNOS acting as a key molecular locus [13]
The present study has demonstrated the beneficial postprandial actions of LC n-3 PUFA on endothelial function to be strongly influenced by a common polymorphism in the eNOS gene and by gender
Summary
Our objective was to determine whether the endothelial nitric oxide synthase (eNOS) Glu298Asp polymorphism influences vascular response to raised NEFA enriched with saturated fatty acids (SFA) or long-chain (LC) n-3 polyunsaturated fatty acids (PUFA). Effects of fat composition appear to be genotype and gender dependent, with the greatest difference in vasodilatory response to the two fat loads seen in the Asp298 females.—Thompson, A. Glu298Asp polymorphism influences the beneficial effects of fish oil fatty acids on postprandial vascular function. The key component in the regulation of vascular homeostasis is nitric oxide (NO), a potent vasodilator produced by endothelial nitric oxide synthase (eNOS).While a number of mechanisms may be responsible for mediating dietary effects, the final common pathway appears to be via fatty acid-dependent alterations in either the production or stability of NO, or the action of NO on the smooth muscle layer [8, 12,13,14], with eNOS acting as a key molecular locus [13].
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