Insulin Treatment Inhibits PAI-1 Production in NIDDM Patients with Endothelial Dysfunction

• Published in: Clinical and applied thrombosis/hemostasis 1998-10, Vol.4 (4), p.250-252
• Main Authors: Galajda, Peter, Baláž, Dušan, Martinka, Emil, Mokán, Marian, Kubisz, Peter
• Format: Article
• Language: English
• Subjects: Insulin; Variance analysis
• ISSN: 1076-0296; 1938-2723
• DOI: 10.1177/107602969800400406

We examined 34 non-insulin-dependent diabetes mellitus (NIDDM) patients treated with sulfonylurea regimens, 24 NIDDM patients with 2-3 months long-acting insulin treat ment and 19 age-matched normoinsulinemic healthy controls. NIDDM patients were divided into two subgroups, with and without endothelial dysfunction according to von Willebrand factor level 0.14 IU/mL. There were significant differences in PAI-1 levels among patients without endothelial dysfunction treated by sulfonylurea agents (median 48.1, range 14-108 ng/ mL) or insulin (27.9, 2-53 ng/mL) and patients with endothe lial dysfunction treated by sulfonylurea regimens (80.7, 43-217 ng/mL) or insulin, respectively, (16.7, 7-34 ng/mL) (analysis of variance p < .001). NIDDM subgroups were not different in metabolic parameters (C-peptide and triglyceride levels, body mass index) and platelet activation marker (platelet factor 4 values). von Willebrand Factor and thrombomodulin levels were elevated in groups with endothelial dysfunction (analysis of variance p < .001, p = .025, respectively). Insulin treatment was accompanied by decreased PAI-1 levels especially in pa tients with endothelial dysfunction. Insulin is the inhibitor of endothelial PAI-1 production induced by cytokines. Therefore, we suggest that long-term insulin application may decrease PAI-1 levels by direct inhibitive action on the endothelial PAI-1 compartment. This hypothesis requires further research.