title: Postprandial recruitment of neutrophils may contribute to endothelial dysfunction.
abstract: Atherosclerosis is a low-grade inflammatory disease involving leukocytes, lipids, and glucose leading to endothelial dysfunction. Since activation of neutrophils by triglycerides and glucose has been described in vitro, we hypothesized that the postprandial phase is an inflammatory state affecting leukocytes, possibly contributing to endothelial dysfunction. We measured postprandial blood leukocyte counts, cytokines, hydroperoxides (HPOs), and flow-mediated vasodilation (FMD) in eight healthy males (age 23 +/- 2 years) after a FAT (50 g/m2) and GLUCOSE challenge (37.5 g/m2), a combination of both (MIXED test), and after WATER. All tests, except WATER, resulted in significantly impaired FMD (10% reduction) between t = 1 h and t = 3 h, accompanied by a significant increase of neutrophils (59% after FAT and 28% after GLUCOSE and MIXED), total plasma HPOs (15 to 31% increase), and plasma interleukin-8 (IL-8) (50-130% increase). WATER did not affect FMD, neutrophils, HPOs, or IL-8. Lymphocytes increased gradually in all tests (40-70% increase at t = 10 h compared with t = 0; P < 0.005), paralleling a gradual 3- to 5-fold interleukin-6 increase. Monocyte and erythrocyte counts did not change in any test. In conclusion, the neutrophil increment during postprandial lipemia and glycemia with concomitant IL-8 and HPO increases may contribute to endothelial dysfunction. Lymphocyte increment is a nonspecific diurnal process. Postprandial intravascular inflammatory changes may be relevant for the pathogenesis of atherosclerosis.
authors.affiliation: Department of Vascular Medicine, University Medical Center, Utrecht, The Netherlands.
authors.forename: A J H H M
authors.initials: AJ
authors.lastname: van Oostrom
authors.forename: T P
authors.initials: TP
authors.lastname: Sijmonsma
authors.forename: C
authors.initials: C
authors.lastname: Verseyden
authors.forename: E H J M
authors.initials: EH
authors.lastname: Jansen
authors.forename: E J P
authors.initials: EJ
authors.lastname: de Koning
authors.forename: T J
authors.initials: TJ
authors.lastname: Rabelink
authors.forename: M
authors.initials: M
authors.lastname: Castro Cabezas
mesh_terms: D000328:Adult; D001161:Arteriosclerosis / Q000139:chemically induced / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*; D001786:Blood Glucose / Q000032:analysis; D004041:Dietary Fats / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000473:pathology*; D005215:Fasting; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005947:Glucose / Q000008:administration & dosage / Q000494:pharmacology; D006801:Humans; D006861:Hydrogen Peroxide / Q000097:blood; D007249:Inflammation / Q000378:metabolism; D007328:Insulin / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D007958:Leukocyte Count; D008297:Male; D008954:Models, Biological; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism*; D019518:Postprandial Period / Q000502:physiology*; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D004041:Dietary Fats; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D015850:Interleukin-6; D016209:Interleukin-8; D014280:Triglycerides; D006861:Hydrogen Peroxide; D005947:Glucose