Thromb Haemost 1989; 61(03): 370-373
DOI: 10.1055/s-0038-1646598
Original Article
Schattauer GmbH Stuttgart

Increased Plasminogen Activator Inhibitor Activity in Non Insulin Dependent Diabetic Patients – Relationship with Plasma Insulin

I Juhan-Vague
1   The Laboratory of Haematology, CHU Timone, Marseille, France
,
C Roul
1   The Laboratory of Haematology, CHU Timone, Marseille, France
,
M C Alessi
1   The Laboratory of Haematology, CHU Timone, Marseille, France
,
J P Ardissone
2   The Laboratory of Biochemistry, CHU Timone, Marseille, France
,
M Heim
3   The Department of Internal Medicine, CHU Timone, Marseille, France
,
P Vague
4   The Department of Diabetology, CHU Timone, Marseille, France
› Institutsangaben
Weitere Informationen

Publikationsverlauf

Received 30. November 1988

Accepted after revision 30. Januar 1989

Publikationsdatum:
24. Juli 2018 (online)

Summary

Type 2 diabetic patients are known to frequently have a high insulin level and were recently described as having high plasminogen activator inhibitor (PAI) activity, compared to normal controls. As we have shown in several clinical conditions (normal subjects, obese patients, angina pectoris patients) that plasma PAI activity was linked with plasma insulin, we have studied in 38 type 2 diabetic patients the relationship between PAI activity, insulin and other parameters. Patients showed higher level of PAI activity, as well as plasma glucose, insulin, triglyceride, cholesterol and Apolipoprotein B levels than normal controls; highest values were observed with diabetic patients also affected by coronary artery disease. A significant correlation was found between PAI activity and insulin (r = 0.60, p <0.001), body mass index (r = 0.32, p <0.05) and Apolipoprotein B (r = 0.33, p <0.05). The two latter correlations disappeared after adjustment for insulin.

These results are in agreement with our previous report showing an in vitro effect of insulin on the synthesis of PAI by a hepatocellular cell line. Hyperinsulinemia presented by type 2 diabetic patients may increase the hepatic synthesis of PAI, inducing an hypofibrinolysis, which could play a role in the development of the vascular complications.

Attempts to reduce hyperinsulinemia could have a favorable effect by lowering PAI activity.

 
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