It is a matter of debate whether postprandial activation of blood coagulati
on factor VII (FVII) is associated with an increased risk of thrombosis. To
clarify this question, an animal model in which consequences of dietary FV
II activation can be studied in a more detailed way would be an important t
ool. We studied postprandial FVII activation in seven non-fasting Gottingen
minipigs, Intralipid (4 g/kg) was administered through a gastric tube in t
wo fractions at 9.00 a.m. (one-third of total dose) and 10.30 a.m. (two-thi
rds of total dose). Blood samples were drawn 0.5 h before (baseline) and 2,
3, 3.5, 4, 5, and bh after the first fat load Triglycerides, activated FVI
I (FVIIa), FVII coagulant activity (FVIIc), FVII amidolytic activity (FVIIa
m) and prothrombin fragment 1 + 2 (F1 + 2) were analysed in plasma samples.
Median plasma triglycerides were significantly raised from 0.67 mmol/l (ba
seline) to 2.56 mmol/l 5 h postprandially (P < 0.001). There were no signif
icant changes in FVIIa (9.6 U/l at baseline), FVIIam (142% at baseline) and
F1 + 2 (0.13 nmol/l at baseline). FVIIc decreased from 141% at baseline to
114% 6 h postprandially (P<0.001). As a high-fat meal does not seem to act
ivate blood coagulation FVII in minipigs, the pig is apparently not a relev
ant model for the study of dietary FVII activation and thrombin generation.
(C) 2001 Lippincott Williams & Wilkins.