Thromb Haemost 2002; 87(03): 477-482
DOI: 10.1055/s-0037-1613028
Review Article
Schattauer GmbH

Factor VII Activation, Apolipoprotein A-I and Reverse Cholesterol Transport: Possible Relevance for Postprandial Lipaemia

Autoren

  • G. J. Miller

    1   MRC Epidemiology and Medical Care Unit, Wolfson Institute of Preventive Medicine, London, UK
  • C. J. Cooke

    2   Department of Cardiovascular Biochemistry, St Bartholomew’s and Royal London School of Medicine and Dentistry, London, UK
  • M. N. Nanjee

    2   Department of Cardiovascular Biochemistry, St Bartholomew’s and Royal London School of Medicine and Dentistry, London, UK
  • D. J. Howarth

    1   MRC Epidemiology and Medical Care Unit, Wolfson Institute of Preventive Medicine, London, UK
  • J. A. Cooper

    1   MRC Epidemiology and Medical Care Unit, Wolfson Institute of Preventive Medicine, London, UK
  • I. P. Stepanova

    2   Department of Cardiovascular Biochemistry, St Bartholomew’s and Royal London School of Medicine and Dentistry, London, UK
  • J. H. Morrissey

    3   Department of Biochemistry, University of Illinois College of Medicine, Urbana, IL, USA
  • N. E. Miller

    2   Department of Cardiovascular Biochemistry, St Bartholomew’s and Royal London School of Medicine and Dentistry, London, UK
Weitere Informationen

Publikationsverlauf

Received 24. Juli 2001

Accepted after resubmission 05. Dezember 2001

Publikationsdatum:
14. Dezember 2017 (online)

Summary

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.