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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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Publication History

Publication Date:
21 June 2005 (online)

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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

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