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
AUTHORS (7)
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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