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Papers In Press, published online ahead of print December 16, 2002
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Vascular Medicine, G.02.405, University Medical Center Utrecht, Utrecht 3508 GA
Corresponding Author: a.vanoostrom{at}azu.nl
Atherosclerosis is a low-grade inflammatory disease involving leukocytes, lipids and glucose, leading to endothelial dysfunction. Since activation of neutrophils by triglycerides (TG) 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 and flow mediated vasodilation (FMD) in eight healthy males (age 23±2yrs) after a FAT (50g/m²) and GLUCOSE challenge (37.5g/m²), a combination of both (MIXED test) and after WATER. All tests, except WATER, resulted in significantly impaired FMD (10% reduction) between t=1h and t=3h, accompanied by a significant increase of neutrophils (59% after FAT and 28% after GLUCOSE and MIXED), total plasma hydroperoxides (15 to 31% increase) and plasma interleukin-8 (50-130% increase). WATER did not affect FMD, neutrophils, hydroperoxides or IL-8. Lymphocytes increased gradually in all tests (40-70% increase at t=10h compared to 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 glycaemia with concomitant interleukin-8 and hydroperoxide increases may contribute to endothelial dysfunction. Lymphocyte increment is a non-specific diurnal process. Postprandial intravascular inflammatory changes may be relevant for the pathogenesis of atherosclerosis.
Revised on December 12, 2002
Accepted on December 16, 2002
Postprandial recruitment of neutrophils may contribute to endothelial dysfunction
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