The activation of factor VII in citrated plasma by charged long-chain saturated fatty acids at the interface of large triglyceride-rich lipoproteins

Effect of long-term olive oil dietary intervention on postprandial triacylglycerol and factor VII metabolism

“…The hydrolysis of TRLs is thought to activate factor VII (19) and there has been considerable research into the effects of test meals and background dietary fat composition on postprandial factor VII activity. Although in vitro studies suggested lesser activation of factor VII by oleic than by stearic acid (20), in vivo studies showed that test meals providing different proportions of SFAs, MUFAs, and polyunsaturated fatty acids (PUFAs) activated factor VII to similar extents (17,21). Mitropoulos et al (19) showed that mean diurnal factor VII activity was lower after an unsaturated fatty acid diet than an SFA diet, but in that study the composition of the test meal was that of the background diet.…”

Influences of lipid and non‐lipid nutritional parameters on factor VII coagulant activity in normal subjects: the Nove Study

“…These authors demonstrated that mechanisms different from the classical tissue factor-mediate pathway can also operate in the activation of FVII. In particular, longchain saturated fatty acids (SFAs) (mainly stearic acid) in the interface of lipoprotein particles provide a negatively charged surface for the initiation of the contact system of coagulation, leading consequently to the activation of factor VII (observed as an increase in FVII c [6]. This property, not shared by unsaturated FAs, has been claimed to explain the well-known univariate association between FVII c ) and plasma triglycerides and cholesterol commonly found in cross-sectional epidemiological studies [25], suggesting that lipoprotein lipid concentrations per se are not primarily responsible for changes in FVII c .…”

“…FAs are considered to be of great importance among the several dietary factors associated with the incidence of CHD [4]. Early in vitro studies reported a prothrombotic effect of stearic acid (C 18 : 0) and other saturated fatty acids (SFAs) [5]; subsequently, the activation of the contact system of coagulation and an increase in FVII c when citrated plasma is incubated in presence of micellar stearic acid have been demonstrated [6]. More recently, two interventional studies with experimental diets in small samples of healthy subjects have given opposite results.…”

Diet and blood coagulation factor VII—a key protein in arterial thrombosis

“…The other hypothesis is based on experiments showing that FVII and FX adhere to TRLP (chylomicrons and VLDL) which might make them less available for catabolic degradation, thus raising their plasma concentration (Sousa et al, 1988(Sousa et al, , 1989. This hypothesis is challenged by the fact that patients with lipoprotein lipase (LPL) de®ciency and massive hypertriglyceridaemia have normal FVIIag levels (Mitropoulos et al, 1992). Both hypotheses are further challenged by the fact that dietary changes in fasting triglycerides and FVIIc may be dissociated or even opposed (Schmidt et al, 1990(Schmidt et al, , 1992Marckmann et al, 1993a.…”

“…In vitro studies indicate that lipolysis of TRLP promotes the activation of FXII to FXIIa (Mitropoulos & Esnouf, 1991;Mitropoulos et al, 1989bMitropoulos et al, , 1992Mitropoulos et al, , 1993. Subsequently, FXIIa might cleave single-chain FVII to FVIIa, thus forming the link from postprandial plasma triglycerides to FVIIa.…”