According to the National Cholesterol Education Panel ATP-III guidelines, the primary management of subjects with MetS involves therapeutic lifestyle changes including decreasing intake of saturated fat, cholesterol, trans fat, and increasing physical activity and addition of sterols and fiber in the diet [12
]. Postprandial lipemia is an independent risk factor for heart disease [4
]. Oxidative stress and inflammation play a pivotal role in atherogenesis. High-fat meals seem to be particularly damaging to the vasculature. Because many Americans consume an energy-dense, high-fat breakfast and not the AHA-recommended heart-healthy breakfast, we wished to test the acute effects of these 2 meals on biomarkers of oxidative stress and inflammation. In this study, we provide novel data in subjects with MetS that, in comparison to an AHA meal, a high-fat, high-energy, high-salt meal (the FFS meal), results in significant augmentation in biomarkers of oxidative stress in the postprandial state. This could be due to the increase in fat or increase in energy or the combination of the two.
Previous studies have shown that a carbohydrate-restricted diet results in increased weight loss, and improvement in insulin sensitivity and triglycerides in patients with MetS or diabetes that are severely obese when compared to an energy- and fat-restricted diet [13
]. They did not assess effects of these diets on biomarkers of oxidative stress and inflammation. However, in this study, we have examined the acute effects of a high-fat, energy-dense breakfast compared to a heart-healthy breakfast on biomarkers of oxidative stress and inflammation, and chronic effects will be examined in future studies comparing high-fat vs low-fat isocaloric diets on biomarkers of oxidative stress and inflammation.
With regard to postprandial oxidative stress, Ursini et al [14
] previously demonstrated that a test meal (English breakfast providing 11% protein, 34% carbohydrate, and 55% fat, approximately 5021 kJ [1200 kcal]) in 9 healthy males resulted in significant 123% postprandial increases in plasma lipid peroxides at 2 hours after the meal. In the present study, there was a similar significant increase in postprandial lipid peroxides, which was accentuated with the FFS meal compared to the AHA meal. Furthermore, in the Ursini study, they only examined one point postprandially in normal healthy subjects. Here, we have compared 2 different meals on postprandial oxidative stress over an 8 hour period in subjects with MetS.
Oxidative stress appears to be an important mechanism by which postprandial lipemia alters vascular function. However, only one study has investigated directly the effect of an oral prooxidant lipid challenge on vascular function. Consumption of a meal containing 65 g fat used repeatedly in deep fat frying, and rich in lipid hydroperoxides, produced a sevenfold decrease in endothelium-dependent flow-mediated dilation, whereas no effect was found with the same amount of unused cooking fat [15
With regard to cytokines, Esposito et al [16
] showed that the consumption of a high-fat meal was associated with increased IL-18 and decreased adiponectin concentration, whereas there was no effect on plasma IL-8 in healthy subjects. However, both postprandial oxidative stress and inflammatory cytokines were not examined, and subjects with MetS were not studied. Lundman et al [17
] recently studied the effect of a high fat meal on IL-6 levels. While IL-6 levels increased, they also failed to find any significant differences postprandially between CAD subjects and controls. Similarly, Motton et al [18
] investigated the effect of a high-glycemic vs low-glycemic index meal on postprandial monocyte cytokines and also failed to observe any significant differences. In the present study, among the cytokines, only the increase in IL-1β
release was significantly increased postprandially after the FFS meal vs the AHA meal.
In summary, we demonstrate for the first time in subjects with MetS that consumption of an energy-dense, high-fat, FFS breakfast results in increased postprandial oxidative stress. We have not speculated if this increased postprandial oxidative stress is due to the increased energy content or due to the high fat content of the diet or both, and this will be examined in future studies. Future studies will examine mechanisms for this increased postprandial oxidative stress and test the effect of therapeutic lifestyle changes and nutritional interventions, especially in the postprandial state.