Endotoxin May Not Be the Major Cause of Postprandial Inflammation in Adults Who Consume a Single High-Fat or Moderately High-Fat Meal. Issue 5 (10th February 2020)

• Record Type: Journal Article
• Authors: Mo, Zhenzhen; Huang, Shurong; Burnett, Dustin J; Rutledge, John C; Hwang, Daniel H
• Is Part Of: Journal of nutrition. Volume 150:Issue 5(2020)
• Page Start: 1303
• Page End: 1312
• Publication Date: 2020-02-10
• Subjects: high-fat diet -- diet and dietary lipids -- diet effects/lipid metabolism -- lipase/lipoprotein -- toll-like receptor -- macrophages/monocytes -- plasma cytokines -- inflammation -- postprandial metabolic endotoxemia -- clinical trials; Nutrition -- Periodicals; Diet -- Periodicals; 613.205
• DOI: 10.1093/jn/nxaa003
• Languages: English
• ISSNs: 0022-3166

Abstract

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.