High-fat, energy-dense, fast-food–style breakfast results in an increase in oxidative stress in metabolic syndrome

Abstract

The metabolic syndrome (MetS) is associated with an increased incidence of diabetes and coronary heart disease. Postprandial lipemia is a prominent feature of dyslipidemia in both type 2 diabetes mellitus and MetS and is also associated with coronary heart disease. Oxidative stress and inflammation are pivotal in all stages of atherosclerosis; however, there is a paucity of data on postprandial oxidative stress and inflammation in subjects with MetS. Thus, the primary aim of this study was to compare the postprandial effects of an energy-dense, high-fat, fast-food-style (FFS) meal with an American Heart Association (AHA)-recommended heart-healthy meal on biomarkers of oxidative stress and inflammation in subjects with MetS. A total of 11 subjects with MetS completed the study. Glucose levels were significantly increased 2 hours after both FFS and AHA diets (P <.0001), and high-density lipoprotein cholesterol levels significantly decreased in FFS diet but not in the AHA diet (P for interaction <.05). Total triglyceride levels significantly increased postprandially only in the FFS meal but not in the AHA meal (P for interaction =.03). Plasma thiobarbituric acid reactive substances and malondialdehyde + hydroxynonenal increased significantly with time in both dietary groups, and the postprandial increase was greater in the FFS diet compared to the AHA diet (P <.0005). Serum high-sensitivity C-reactive protein, interleukin 6, and tumor necrosis factor levels did not change with time or dietary treatment. The postprandial increase in interleukin 1b was significantly higher with the FFS meal, thus resulting in significant differences between both treatments (P for interaction = .03). Thus, in subjects with MetS, consumption of an energy-dense, fatty meal (FFS breakfast) results in increased postprandial oxidative stress compared to a heart-healthy meal (AHA).

Fast food consumption and the risk of metabolic syndrome after 3-years of follow-up: Tehran Lipid and Glucose Study

“…37 Another cross-sectional study also reported that dietary energy density was an independent predictor of obesity, elevated fasting insulin levels, and the metabolic syndrome in adults. 38 High content of fats, cholesterol, saturated and trans fatty acids in fast foods also considered as threatening factor could lead to postprandial metabolic disorders including dyslipidemia, subclinical inflammatory process and oxidative stress, 39 and also long term abdominal fat gain, insulin resistance and hypertension. [40][41][42][43] While consumption of 5 grams trans fat per day may increase the risk of ischemic heart disease up to 25%, the trans fatty acid content of only one fast food meal was reported several times of recommended amount by dietary guidelines.…”

Lipid Peroxidation by-Products and the Metabolic Syndrome

“…After consumption of an energy-dense (i.e. high-fat) diet, plasma HNE levels increase rapidly and significantly within minutes (Devaraj et al, 2008). When consumed regularly, this diet promotes obesity, which suggests a role for HNE very early in the development of obesity.…”

Postprandial oxidative stress is modulated by dietary fat in adipose tissue from elderly people

“…The postprandial state is a stressful condition in which an increase in oxidative stress takes place (Cardona et al 2008;Devaraj et al 2008;Ursini and Sevanian 2002). Postprandial oxidative stress is characterized by an imbalance between the production of ROS and their elimination by the antioxidant system (Durackova 2009).…”

“…Postprandial oxidative stress is characterized by an increase in oxidative stress biomarkers after the intake of a meal (Cardona et al 2008;Devaraj et al 2008;Ursini and Sevanian 2002), which is extremely important, as humans spend most of their time in the postprandial state (de Koning and Rabelink 2002). In line with this, we previously demonstrated that a MUFA-rich diet improves plasma postprandial oxidative stress parameters compared to an SFA-rich diet, and that low-fat diets have an intermediate effect relative to the MUFA-rich and SFA-rich diets (PerezMartinez et al 2010).…”