Alimentary lipemia enhances the membrane expression of platelet P-selectin without affecting other markers of platelet activation.
The present study was conducted to determine whether alimentary lipemia alters platelet activity in vivo. Normolipidemic volunteers were given a fatty meal and platelet function was assessed before, and 3 and 6 h after the meal. Platelet aggregability and secretion was determined using whole blood flow cytometry (expression of platelet P-selectin and fibrinogen binding), filtragometry ex vivo (reflecting platelet aggregability in vivo) and by measurements of platelet specific products in plasma (beta-thromboglobulin and platelet factor 4). Plasma triglycerides increased from 0.8 (0.6:1.1; median, 25th and 75th percentiles) to 1.7 (1.0:2.3) mmol/l at 3 h and returned to baseline after 6 h (P < 0.001, one-way ANOVA). Apo B-100 and apo B-48 were both markedly increased 3 h postprandially in the Sf 60-400 fraction (large VLDLs, P < 0.001 for both), whereas the Sf 20-60 (small VLDLs) and Sf 12-20 fractions (IDL) did not change. The platelet function assessments revealed that the percentage of platelets expressing P-selectin increased by 40% (5%; 64%) after 3 h and by 51% (- 7%; 85%) 6 h postprandially in unstimulated samples (P < 0.05 for both). In samples stimulated by ADP in vitro P-selectin expression increased by 45% (6%; 58%) after 3 h and by 30% (12%; 58%) (P<0.01 for both) after 6 h at 0.1 microM. Platelet P-selectin expression was less influenced at higher ADP concentrations. The plasma levels of beta-thromboglobulin (approximately 20 ng/ml) and platelet factor 4 (approximately 0.3 ng/ml) were not affected by the fat load. Flow cytometric analyses of fibrinogen binding and filtragometry measurements also failed to reveal any postprandial alterations. The present finding of enhanced platelet P-selectin expression suggests that platelets are mildly sensitized postprandially. Whether this is of importance for thrombus formation and atherosclerosis needs to be studied further.
Bröijersén
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A
Department of Laboratory Medicine, Karolinska Institute & Hospital, Stockholm, Sweden. Anders.Broijersen@labmed.ki.se
Karpe
F
F
Hamsten
A
A
Goodall
A H
AH
Hjemdahl
P
P
D000328:Adult; D001055:Apolipoproteins B / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000737:chemistry / Q000502:physiology; D002462:Cell Membrane / Q000737:chemistry / Q000378:metabolism; D003627:Data Interpretation, Statistical; D004036:Diet, Atherogenic; D004041:Dietary Fats / Q000378:metabolism; D006801:Humans; D006949:Hyperlipidemias / Q000503:physiopathology; D015228:Hypertriglyceridemia / Q000503:physiopathology*; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology; D008297:Male; D019007:P-Selectin / Q000096:biosynthesis*; D015539:Platelet Activation / Q000502:physiology*; D010978:Platelet Factor 4 / Q000032:analysis; D019518:Postprandial Period / Q000502:physiology; D013997:Time Factors; D014280:Triglycerides / Q000097:blood / Q000502:physiology*; D001620:beta-Thromboglobulin / Q000032:analysis
D001055:Apolipoproteins B; D015415:Biomarkers; D004041:Dietary Fats; D008055:Lipids; D008074:Lipoproteins; D019007:P-Selectin; D014280:Triglycerides; D001620:beta-Thromboglobulin; D010978:Platelet Factor 4