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Differential response of plasma plasminogen activator inhibitor 1 after weight loss surgery in patients with or without type 2 diabetes

Journal article
Authors Karin Mossberg
Dimitri J. Pournaras
Richard Welbourn
Carel W le Roux
Helén Brogren
Published in Surgery for Obesity and Related Diseases
Volume 13
Pages 53-57
ISSN 1550-7289
Publication year 2017
Published at Institute of Clinical Sciences, Department of Gastrosurgical Research and Education
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 53-57
Language en
Links doi.org/10.1016/j.soard.2016.03.007
Keywords Bariatric surgery, Gastric bypass, Obesity, PAI-1, Type 2 diabetes
Subject categories Diabetology, Endocrine surgery

Abstract

© 2017 American Society for Bariatric Surgery Background Obesity and type 2 diabetes (T2D) are associated with a suppression of fibrinolysis and an increased risk of intravascular thrombi because of elevated plasma plasminogen activator inhibitor 1 (PAI-1). Objectives The aim was to investigate PAI-1 levels in obese patients in the early phase after bariatric surgery, before any weight loss, and in the late phase, to identify the impact of reduced adipose mass versus weight loss independent effects on PAI-1 levels. We also studied the impact of T2D on the rate of PAI-1 reduction. Settings Twelve obese patients with and without T2D (n = 6) who were scheduled for surgery at a designated Center of Excellence. Methods Plasma PAI-1 antigen was measured by enzyme-linked immunosorbent assay (ELISA) preoperatively and at 4 and 42 days after gastric bypass surgery. Results In the early phase, plasma PAI-1 was significantly decreased by 53% (P = .023). This difference did not remain significant in the late phase. However, PAI-1 levels in T2D and non-T2D patients were significantly different (P = .005). In non-T2D patients, plasma PAI-1 levels decreased significantly in both early and late phases (P = .038). Interestingly, in the T2D group, the PAI-1 levels tended to increase in the late phase and differed significantly from the non-T2D group. Conclusion We report decreased PAI-1 levels in the immediate postoperative period after gastric bypass, indicating that a mechanism not related to the fat mass regulates the PAI-1 levels. Additionally, there may be a difference in PAI-1 levels between T2D and non-T2D patients 42 days postoperatively. Further studies are required to verify this difference and to elucidate the specific mechanisms responsible for PAI-1 synthesis.

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