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

Artikel i vetenskaplig tidskrift
Författare Karin Mossberg
Dimitri J. Pournaras
Richard Welbourn
Carel W le Roux
Helén Brogren
Publicerad i Surgery for Obesity and Related Diseases
Volym 13
Sidor 53-57
ISSN 1550-7289
Publiceringsår 2017
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för gastrokirurgisk forskning och utbildning
Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor 53-57
Språk en
Länkar doi.org/10.1016/j.soard.2016.03.007
Ämnesord Bariatric surgery, Gastric bypass, Obesity, PAI-1, Type 2 diabetes
Ämneskategorier Diabetologi, Endokrin kirurgi

Sammanfattning

© 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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