Influence of fatty acid chain length and cis/trans isomerization on postprandial lipemia and factor VII in healthy subjects (postprandial lipids and factor VII).

Exaggerated postprandial lipemia is believed to be atherogenic and to influence risk of thrombosis. The postprandial effects on plasma triacylglycerol concentration, factor VII coagulant activity (FVII(c)) and activated FVII concentration (FVII(a)) of five high fat meals (5.2 MJ, 90 g fat) enriched with medium triacylglycerols (MCT, 8:0+10:0), palmitate(16:0), stearate (18:0), elaidate(18:1 trans) and oleate(18:1 cis) were compared with those following a low fat meal (5.2 MJ,10 g fat) in 16 healthy subjects using a randomized crossover design. Postprandial lipemia measured as the area under the curve (AUC arbitrary units) for plasma triacylglycerol concentration (mean+/-SE) was greater following the oleate (5.8+/-1. 05), elaidate (4.3+/-0.79) and palmitate (4.1+/-0.64) meals compared with stearate (2.0+/-0.45) and MCT (1.1+/-0.47) meals. Fatty acid analyses of the chylomicron lipids suggested that approximately one fifth of the dietary stearate was not absorbed. FVII(c) increased following the oleate, elaidate and palmitate meals and fell following the low fat meal; the increase in FVII(c) was correlated with the AUC for plasma TAG (r=0.34; P=0.001). FVII(a) concentration increased following all high fat meals but not following the low fat meal. The increase in FVII(a) at 7 h was greater after the oleate meal than after the stearate and MCT meals. These results do not support the hypothesis that dietary stearate and elaidate are responsible for the postprandial increases in FVII associated with high fat intakes.

Dietary oleic and palmitic acids and postprandial factor VII in middle-aged men heterozygous and homozygous for factor VII R353Q polymorphism.

BACKGROUND: The R353Q genotype is a major determinant of factor VII coagulant (FVIIc) activity, which is associated with an increased risk of ischemic heart disease (IHD) and elevated plasma triacylglycerol concentrations. OBJECTIVE: The objectives were to 1) compare the effects of meals rich in palmitate or oleate with those of a meal low in fat on FVIIc in subjects with moderately elevated plasma nonfasting triacylglycerol concentrations and 2) determine whether the postprandial increase in FVIIc induced by dietary oleate differs in carriers of the Q allele. DESIGN: Fifty-two men aged >52 y with nonfasting plasma triacylglycerol concentrations between 2 and 5.5 mmol/L were randomly assigned to receive isoenergetic (5.1 MJ) meals providing 50 g high-oleate or high-palmitate oils or a low-fat meal providing 15 g high-oleate oil. In a second study, 17 men aged >52 y who were heterozygous for factor VII R353Q polymorphism were age-matched with subjects homozygous for the R allele and their responses to a 50-g, high-oleate meal were measured. RESULTS: FVIIc decreased by 11% after the low-fat meal. FVIIc increased by 9% and FVIIa (the activated form of FVII) increased by 55% after the high-oleate meal, whereas FVIIc did not change but FVIIa increased by 25% after the high-palmitate meal. Fasting FVIIc and FVIIa concentrations were 24% and 48% lower, respectively, in men with the RQ genotype than in men with the RR genotype but increased postprandially in both groups with no evidence of a genotype interaction. CONCLUSIONS: A high-fat meal rich in oleate increases FVIIa, whereas a low-fat meal does not, in men at high risk of IHD, independent of R353Q genotype.

Influence of variation in fat composition on haemostatic variables.

The effects of saturated fatty acids on platelet function remain uncertain although hypercholesterolaemia is associated with increased platelet aggregrability. The consumption of n-3 fatty acids as fish oils leads to a reduction in the concentration of arachidonic acid (20:4n-6) in platelets and endothelial cells and its replacement with eicosapentaenoic acid (20:5n-3, EPA) and docosahexaenoic acid (22:6n-3, DHA). This change is accompanied by a prolongation of template bleeding time. The effect of replacing arachidonic acid with EPA and DHA is to decrease the production of thromboxane A2 and increase that of the antiaggregatory prostacyclins. Despite the association between plasma triglyceride concentrations and impaired fibrinolytic activity, there is little evidence to suggest that the type of fat influences PAI-1, tPA or global markers of fibrinolysis. Some studies have reported that plasma fibrinogen concentration may be decreased by n-3 fatty acids but a large number have found no effect. Plasma triglyceride concentrations are strongly associated with increased factor VII coagulant activity (FVIIc). Despite their well known hypotriglyceridaemic effects, n-3 fatty acids do not decrease FVIIc. Postprandial activation of FVII is now well recognised and oleic acid appears to be among the most potent activators. These effects are, however, dose related. In view of their potentially prothrombotic influence, it would be wise to caution against high intakes of fat in the middle-aged and elderly population who are most at risk.