Postprandial recruitment of neutrophils may contribute to endothelial dysfunction

Adult Blood Glucose Male 0301 basic medicine Time Factors Arteriosclerosis Neutrophils QD415-436 Fatty Acids, Nonesterified Biochemistry Models, Biological Leukocyte Count 03 medical and health sciences endothelial function Humans Insulin hydroperoxides triglycerides Inflammation Interleukin-6 Interleukin-8 Fasting Hydrogen Peroxide Postprandial Period Dietary Fats cytokines 3. Good health Glucose Endothelium, Vascular
DOI: 10.1194/jlr.m200419-jlr200 Publication Date: 2003-03-03T21:04:14Z
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.
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