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
REFERENCES
1 , and BMI are closely associated in human adipose tissue during morbid obesity.
Diabetes.
2000;
49
1374-1380
