Food Lipids: Chemistry, Nutrition, and Biotechnology

as compared with a diet rich in butterfat. In a second study, both thrombin- and
ADP-induced aggregation of platelet-rich plasma was significantly higher with a high
oleic acid sunflower oil diet compared with a rapeseed oil diet [67]. The authors
concluded that especially the ratio of linoleic acid to �-linolenic acid of the diets
was an important determinant for platelet reactivity. It was postulated that this higher
ratio on diets rich in sunflower oil will result in higher concentrations of arachidonic
acid, the substrate for TxA 2 production, in platelet phospholipids. According to this
hypothesis, oleic acid should lower platelet aggregation, as the proportion of arachidonic
acid in platelet phospholipids is decreased following oleic acid consumption.
However, this was not supported by the results from a small study with only three
or four subjects per diet group on the effects of dietary linoleic acid compared with
those of oleic acid. In this study, the oleic acid diet increased ADP- and collageninduced
platelet aggregation [68].
Effects of specific saturated fatty acids on stable metabolites of TxA 2 and PGI 2
—TxB 2 and 6-keto-PGF 1�, respectively—in urine have been investigated for diets
rich in stearic acid provided by cocoa butter or milk chocolate, as compared with
diets rich in butterfat [69]. Although milk chocolate consumption decreased and
butterfat intake increased the arachidonic acid contents of platelet phospholipids, the
three diets did not change the concentrations of TxB 2 and 6-keto-PGF 1� in urine.
B. Coagulation
Several pathways for blood coagulation exist. The tissue factor pathway of blood
coagulation, previously known as the extrinsic pathway of blood coagulation, appears
to be the most important one. The factors involved in this pathway are depicted in
a simplified scheme in Figure 14. Most coagulation factors are mainly present in
inactivated form, except for factor VII, of which 1% circulates as activated factor
VII (factor VIIa) [70]. However, Figure 14 only shows the activated coagulation
factors, except for factor VII.
Thrombus formation in vivo is initiated when factor VII or factor VIIa contacts
thromboplastin tissue factor, expressed, for example, after vessel injury or inflammation.
A tissue factor, such as thromboplastin, is a procoagulant that is expressed
only on activated endothelium. Once bound, factor VII is rapidly activated into factor
VIIa. The complex of factor VIIa with tissue factor initiates a cascade of reactions,
which ultimately results in the conversion of factor X into factor Xa and the generation
of thrombin from prothrombin. Thrombin finally cleaves fibrinogen into fibrin,
that stabilize a thrombus. However, thrombin also inhibits some coagulation
factors, and the coagulation cascade is thus inhibited by one of its end products so
as to prevent uncontrolled formation of fibrin.
The coagulation cascade is further regulated by the action of coagulation inhibitors.
An important inhibitor of coagulation is the tissue factor pathway inhibitor
(TFPI), whic inhibits the activity of the tissue factor–factor VIIa complex and TFPI
therefore prevents further activation of the coagulation cascade. The tissue factor–
factor VIIa complex is also inhibited by antithrombin III, which also suppresses the
activation of thrombin and other activated coagulation factors [71].
1. Measurement of Coagulation
Most assays measure the total amount (e.g., factor VII–antigen or fibrinogen concentrations)
or the activity of circulating coagulation factors. However, these factors
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