Factor VII activation, apolipoprotein A-I and reverse cholesterol transport: possible relevance for postprandial lipaemia

• Published in: Thrombosis and haemostasis Vol. 87; no. 3; p. 477
• Main Authors: Miller, G J, Cooke, C J, Nanjee, M N, Howarth, D J, Cooper, J A, Stepanova, I P, Morrissey, J H, Miller, N E
• Format: Journal Article
• Language: English
• Published: Germany 01-03-2002
• Subjects: Adult; Antithrombin III; Apolipoprotein A-I - administration & dosage; Apolipoprotein A-I - pharmacokinetics; Apolipoprotein A-I - pharmacology; Biological Transport - drug effects; Cholesterol - metabolism; Cholesterol Esters - blood; Enzyme Activation - drug effects; Factor VII - drug effects; Factor VII - metabolism; Humans; Hyperlipidemias - etiology; Infusions, Parenteral; Kinetics; Lipoproteins, HDL - blood; Lipoproteins, HDL - drug effects; Male; Peptide Hydrolases - blood; Phosphatidylcholines - administration & dosage; Postprandial Period - physiology
• ISSN: 0340-6245
• DOI: 10.1055/s-0037-1613028

Postprandial lipaemia is associated with activation of factor VII (FVII) and efflux of cholesterol from tissues to nascent plasma high density lipoproteins (HDL) containing apolipoprotein A-I (apo A-I). To determine whether FVII activation and cholesterol efflux occur together in other situations, the responses to intravenous infusion of HDL-like apo A-I/phosphatidylcholine discs were measured in 10 healthy men. Disc infusion (40 mg apo A-I/kg body weight) over 4 h was followed by increases in HDL cholesteryl ester and plasma apo A-I (p <0.0001). Significant activation of FVII was apparent during infusion in fasting subjects (p = 0.03), activated FVII averaging 123% of baseline value by 12 h (p <0.0001). Plasma thrombin-antithrombin (TAT) complex increased to 156% of baseline level by 12 h (p >0.05) but individual responses differed considerably. Peak TAT post-infusion was associated inversely with peak HDL triglyceride concentration (p = 0.004). The coagulation responses to disc-infusion may be due to transfer of phosphatidylserine to cell surfaces during cholesterol efflux.