Scope: The aim of this study is to investigate acute postprandial responses to intake of meals typical for Mediterranean and Western diets. Methods: In a randomized crossover design, overweight and obese participants with a risk phenotype for cardiometabolic diseases consumed three different isoenergetic meals: Western diet-like high-fat (WDHF), Western diet-like high-carbohydrate (WDHC), and Mediterranean diet (MED) meal. Blood samples are collected at fasting and 1, 2, 3, 4, 5 h postprandially and analyzed for parameters of lipid and glucose metabolism, inflammation, oxidation, and antioxidant status. Results: Compared to MED and WDHF meals, intake of a WDHC meal results in prolonged and elevated increases in glucose and insulin. Elevations for triglycerides are enhanced after the WDHF meal compared to the MED and the WDHC meal. Glucagon-like peptide-1 and interleukin-6 increase postprandially without meal differences. Apart from vitamin C showing an increase after the MED meal and a decrease after WDHF and WDHC meals, antioxidant markers decrease postprandially without meal differences. Plasma interleukin-1 is not affected by meal intake. Conclusions: Energy-rich meals induce hyperglycemia, hyperlipemia, an inflammatory response, and a decrease in antioxidant markers.

Purpose Low-grade inflammation in obesity is associated with insulin resistance and other metabolic disturbances. In response to high-energy meal intake, blood concentrations of inflammatory markers, glucose and insulin rise. The aim of this study was to examine whether a basal inflammatory state influences postprandial responses. Methods A randomized crossover trial was performed in 60 participants with a cardiometabolic risk phenotype (age 70 ± 5 years; BMI 30.9 ± 3.1 kg/m2). Each participant consumed three different iso-energetic meals (4300 kJ): a Western diet-like high-fat meal (WDHF), a Western diet-like high-carbohydrate meal (WDHC) and a Mediterranean diet-like meal (MED). Blood samples were collected when fasted and hourly for 5 h postprandially and analyzed for glucose, insulin, interleukin-1β (IL-1β), interleukin-6 (IL-6) and endothelial adhesion molecules. Based on fasting serum C-reactive protein (CRP) concentrations, participants were assigned to a high inflammation (CRP ≥ 2.0 mg/L; n = 30) or low inflammation (CRP < 2.0 mg/L; n = 30) group, and postprandial outcomes were compared. Results Plasma IL-6, glucose and serum insulin increased after all meals, while IL-1β and endothelial adhesion molecules were unchanged. The high inflammation group had higher fasting and postprandial IL-6 concentrations than the low inflammation group, although the IL-6 response slope was similar between groups. In response to the WDHC meal, participants in the high inflammation group experienced a higher glycaemic response than those in the low inflammation group. Conclusion A basal proinflammatory state results in higher absolute fasting and postprandial IL-6 concentrations, but the increase in IL-6 relative to basal levels is not different between high and low inflammation groups. Elevated glycaemic response in the high inflammation group may be due to inflammation-induced short-term insulin resistance. The trial was registered at http://www.germanctr.de and http://www.drks.de under identifier DRKS00009861 (registration date, January 22, 2016).

The apolipoprotein E (APOE) polymorphism impacts blood lipids and biomarkers of oxidation and inflammation, contributing to an isoform-dependent disease risk. We investigated the effect of the APOE genotype on postprandial metabolism after consumption of three different isoenergetic (4200 kJ) meals in older adults with a CVD risk phenotype. In a randomized crossover study, participants with metabolic syndrome traits (APOE E3, n = 39; E4, n = 10; mean age, 70 ± 5 years; BMI 31.3 ± 3.0 kg/m2) consumed a Western-like diet high-fat (WDHF), Western-like diet high-carbohydrate (WDHC), or Mediterranean-like diet (MED) meal. Parameters of lipid and glucose metabolism, inflammatory, and oxidative parameters were analyzed in blood samples collected at fasting and 1–5 h postprandially. Data were analyzed by linear mixed models. The magnitude of the IL-6 increase after the WDHF meal was significantly higher in E4 than in E3 carriers (iAUC: E4 = 7.76 vs. E3 = 2.81 pg/mL × h). The time to detect the IL-6 increase was shorter in the E4 group. All meals produced postprandial glycemia, insulinemia, and lipidemia, without differences between the E3 and the E4 groups. IL-1β and oxidized LDL levels did not change postprandially. In conclusion, APOE E4 carriers display increased postprandial inflammation, indicated by higher postprandial IL-6 increase, when compared to non-carriers.

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