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Semin Vasc Med 2005; 5(1): 48-55
DOI: 10.1055/s-2005-871741
Copyright © 2005 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001 USA. Tel: +1(212) 584-4662.

Visceral Fat as a Determinant of Fibrinolysis and Hemostasis

Ilse Mertens1 , Luc F. Van Gaal1
  • 1Department of Diabetology, Metabolism and Clinical Nutrition, Faculty of Medicine, Antwerp University Hospital, University of Antwerp, Antwerp, Belgium
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Publikationsverlauf

Publikationsdatum:
21. Juni 2005 (online)

    Lizenzen und Reprints

ABSTRACT

An increased amount of deep abdominal visceral fat has generally been accepted as an important cardiovascular risk factor, and disturbances in hemostasis and fibrinolysis have been suggested to play a role. Fibrinogen and von Willebrand factor, representatives of the hemostatic system, and plasminogen activator inhibitor 1 (PAI-1), as the most important inhibitor of the fibrinolytic system, have been associated with visceral obesity, with the most convincing evidence found for the involvement of PAI-1. The association with fibrinogen and von Willebrand factor has been suggested to be merely a reflection of the association with inflammation and endothelial dysfunction. The fact that PAI-1 is secreted by adipose tissue has attracted much attention. The increase of PAI-1 in visceral obesity could be because visceral adipose tissue produces more PAI-1 compared with subcutaneous abdominal adipose tissue. The contribution of other cell types such as hepatocytes or endothelial cells is probably more important, with stimulation of PAI-1 production by different components of the metabolic syndrome. PAI-1 secretion by adipose tissue has been suggested to have a more local effect, playing a role in tissue remodeling during the development of obesity.

KEYWORDS

Visceral obesity - fibrinogen - vWF - PAI-1

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 Prof. Dr.
L. F Van Gaal

Department of Diabetology, Metabolism, and Clinical Nutrition

Antwerp University Hospital

Wilrijkstraat 10, B-2650 Edegem, Antwerp, Belgium