APOE ɛ4 Is Associated with Postprandial Inflammation in Older Adults with Metabolic Syndrome Traits

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.

Apple consumption reduces markers of postprandial inflammation following a high fat meal in overweight and obese adults: A randomized, crossover trial

High fat meal-induced postprandial inflammation is exacerbated in overweight and obesity and may contribute to cardiovascular disease (CVD) risk. This study aimed to determine the effects of apples, rich in...

Endotoxin May Not Be the Major Cause of Postprandial Inflammation in Adults Who Consume a Single High-Fat or Moderately High-Fat Meal

ABSTRACT Background Metabolic endotoxemia is considered a cause for high-fat diet (HFD)-induced inflammation. However, convincing experimental evidence in humans is scant. Objective We determined whether a HFD or moderately HFD increases LPS and LPS-mediated cytokine production in the postprandial blood (PPB). Methods Ninety-eight volunteers (age: 37.3 ± 1.5 y) from the cross-sectional phenotyping study (PS) and 62 volunteers (age: 26.8 ± 1.2 y) from the intervention study (IS) consumed a breakfast containing 60% kcal fat (HF) and 36% kcal fat (moderately HF), respectively. For the IS, only the results from the placebo group are presented. Blood samples were probed for LPS-mediated cytokine production by incubating them with LPS inhibitor polymyxin B (PMB) for 24 h at 37°C besides the Limulus amebocyte lysate (LAL) assay. Repeated-measures ANOVA was used to compare the temporal changes of metabolic profiles and treatment outcomes. Results At least 87.5% of the plasma LPS measurements in 32 PS volunteers from each time point were below the LAL assay sensitivity (0.002 EU/mL). PMB suppressed IL-1β (P = 0.035) and IL-6 (P = 0.0487) production in the 3 h PPB of the PS after 24 h incubation at 37°C compared to the vehicle control, suggesting the presence of LPS. However, the amount of LPS did not increase the cytokine concentrations in the 3 h PPB above the fasting concentrations. Such suppression was not detected in the PPB of the IS. Treating whole blood with lipoprotein lipase (LPL) significantly (P < 0.05) increased FFA and cytokine (IL-1β, IL-6, TNF-α) concentrations in both studies. Conclusion LPS may not be the major cause of postprandial inflammation in healthy adults consuming a moderately HF meal (36% kcal fat, similar to the typical American diet) or a HF meal (60% kcal fat). Plasma FFAs may modulate postprandial inflammation. The prevailing concept of HFD-induced metabolic endotoxemia requires careful re-evaluation. The PS was registered at clinicaltrials.gov as NCT02367287 and the IS as NCT02472171.

The Postprandial Effect of Spice Consumption Delivered in a High-Fat Meal on Pro-Inflammatory Cytokine Secretion in Overweight/Obese Men (OR12-06-19)

Objectives Postprandial lipidemia is a risk factor for cardiovascular disease. The postprandial inflammation that occurs concurrently with lipidemia following ingestion of a high-fat meal (HFM) may contribute to this association. Numerous individual spices have anti-inflammatory properties in vitro and in vivo in animal models and humans. However, the effect of consumption of a spice blend on inflammatory mediators has not been examined in humans in a randomized controlled trial. The objective of this study was to investigate the postprandial effect of spice consumption delivered in a HFM on inflammatory cytokine responses. Methods Overweight/obese (BMI ≥25 and ≤35 kg/m2), nonsmoking, men (40–65 years old) with elevated waist circumference (≥94 cm) and at least one other risk factor for cardiovascular disease were recruited for a 3-period crossover study (n = 12). In random order, participants consumed the following dietary interventions: 1) a HFM (1076 kcal, 39% kcal from saturated fat), 2) a HFM containing 2 g of spice blend, or 3) a HFM containing 6 g of spice blend with a ≥3-day washout period between each test meal. The spice blend consisted of black pepper, basil, bay leaf, cinnamon, coriander, cumin, ginger, oregano, parsley, rosemary, red pepper, thyme and turmeric. Participants fasted overnight and blood was collected before, and hourly for four hours after the HFM. Peripheral blood mononuclear cells (PBMCs) were isolated at each time point, and the number of monocytes (CD14+/HLA-DR+) were quantified by flow cytometry. PBMCs were stimulated with lipopolysaccharide (LPS) and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8, MCP-1) were quantified by ELISA in the supernatants. Results Monocyte number (P = 0.001), and the secretion of IL-1β (P = 0.036) and TNF-α (P = 0.046) from LPS-stimulated PBMCs were significantly elevated during the four-hour time period after HFM consumption compared to the baseline. However, the presence of 6 g of spice in the HFM reduced the secretion of IL-6 (P = 0.046), IL-8 (P = 0.031), TNF-α (P = 0.001) and MCP-1 (P = 0.063) from PBMCs at 60 min after the meal. Conclusions Consumption of a HFM containing a spice blend attenuated postprandial inflammation in overweight/obese men. Funding Sources McCormick Science Institute; Penn State Clinical and Translational Science Institute