Increased Platelet Aggregation during Alimentary Hyperlipemia in Normal and Hypertriglyceridemic Subjects

Abstract

The influence of 2 different fatty meals, rich in either saturated or polyunsaturated fatty acids, on platelet aggregation in 7 normolipemic subjects and in 10 patiens with phenotype IV hyperlipemia, was studied. 3 h after ingestion of a saturated- or polyunsaturated-fat-rich meal, plasma triglycerides were similarly increased in both groups. 5 h after ingestion of fat of either origin, the plasma triglyceride level in normal subjects returned almost to the fasting level, whereas in patients with hypertriglyceridemia it was still elevated. Platelet aggregation induced by ADP in platelet-rich plasma significantly increased in the normal group 3 h after both meals, whereas in the patient group it increased only after the saturated-fat-rich meal. These results were not changed 5 h after the meals. Postprandial elevated platelet activity was not correlated with increased plasma triglyceride concentration. No changes were found in washed-platelet aggregation in normal subjects, whereas the patient-derived washed platelets showed increased aggregation after the saturated-fat-rich meal. Plasma chylomicrons prepared from both groups during alimentary hyperlipemia inhibited ADP-induced platelet aggregation as well as thrombin-induced platelet ¹⁴C-serotonin release. This study indicates that the intake of fatty meals induces acute disturbance in platelet aggregation, favoring thrombosis. These changes are more comprehensive in hyperlipemic patients and after a saturated-fat-rich meal.

EPA, but not DHA, decreases mean platelet volume in normal subjects

“…Platelet aggregation induced by ADP (24) and by collagen (25) was significantly increased in normolipemic subjects after fatty meals. Fuhrman et al (24) showed that platelets maintained their hypersensitivity to aggregation 5 h after meals, at a time when plasma TG levels had returned to normal.…”

“…Platelet aggregation induced by ADP (24) and by collagen (25) was significantly increased in normolipemic subjects after fatty meals. Fuhrman et al (24) showed that platelets maintained their hypersensitivity to aggregation 5 h after meals, at a time when plasma TG levels had returned to normal. Chylomicron remnant particles enhanced activation of platelets stimulated with ADP and collagen (42), but native chylomicrons inhibited platelet function (43).…”

“…The eight conditions were: unstimulated or stimulated with collagen, heat or cold, all in the fasting and the fed states. The effect of eating was examined because platelet activation was expected to be greater in the fed than the fasting state (24,25). Three different ex vivo stimuli were included in anticipation that, if EPA or DHA did not activate platelets in the basal state, they might affect platelet response to stimulation.…”

Supplementation of Virgin Coconut Oil Compared with Copra Oil, Olive Oil and Sunflower Oil on Thrombotic Factors in Rats and In Vitro Platelet Aggregation

“…Studies suggest that individual saturated fatty acids differently affect platelet aggregation capacity (Fuhrman et al, 1986;Renaud et al, 1986). There are reports that chain length of fatty acids plays an important role in platelet aggregation and the inhibitory effect on platelet aggregation was increased with increase in chain length up to C 14 (Kitagawa et al, 1984).…”

Postprandial Lipid Metabolism: The Missing Link Between Life-Style Habits and the Increasing Incidence of Metabolic Diseases in Western Countries?~!2009-09-30~!2010-01-26~!2010-03-30~!

“…Other pro-inflammatory and potentially atherogenic effects of postprandial lipoproteins include activation of leukocytes, promoting adhesion to the endothelium and invasion of the artery wall [12,40]. In addition, postprandial lipemia causes pro-thrombotic effects such as increasing coagulant factor VII [41] and plasminogen activator inhibitor type 1(PAI-1) activity [42] and increasing platelet activity [14,43] and aggregation [44].…”