title: Vitamin E intake reduces plasminogen activator inhibitor type 1 in T2DM patients.
abstract: Previous studies hypothesised that vitamin E could protect against coronary heart disease and vascular complications in diabetes, but no studies have been performed regarding its eventual effects on fibrinolysis. Nevertheless, in Type 2 diabetes mellitus (T2DM) a profound reduction in the fibrinolytic activity has been demonstrated to be involved in vascular complications, probably due to plasminogen activator inhibitor type 1 (PAI-1) overproduction. On this basis we aimed to verify whether an antioxidant treatment with vitamin E is able to lower PAI-1 plasma levels in T2DM. Thirteen T2DM patients (9 males and 4 females; mean age+/-SD, 64.4+/-3.3 yr) were selected through strict admission criteria. These patients were treated with vitamin E (500 IU/die) for 10 weeks. Glyco-lipometabolic, oxidative and haemocoagulative parameters were evaluated at baseline and after 5, 10, 30 and 60 weeks. Vitamin E levels at different times were [median (interquartile range)] 6.1 (5.3-7.7), 8.5 (7.3-9.9), 9.7 (8.9-12.9), 5.6 (4.4-6.8), 5.7 (4.5-7.1) microg/ml, respectively. Significant differences were found for PAI-1 antigen (p=0.006), PAI-1 activity (p=0.028), apolipoprotein B (p=0.015) and antioxidant defence, evaluated as ferric reducing ability of plasma (FRAP) values (p=0.005). Particularly, decrements were detected for PAI-1 antigen between baseline and the 10th week (p<0.05), followed by an increase back to basal at the 30th week. Similar behaviour was found for PAI-1 activity. Regarding the antioxidant defence, FRAP values increased until the 30th week (p<0.05) with a decrease at the 60th week. These results demonstrate that vitamin E is able to lower PAI-1 levels in diabetic patients but this effect does not seem related to improvements of glycometabolic data or to the increase in FRAP values, suggesting that PAI-1 overproduction can be decreased by other effects of vitamin E on endothelial cells.
authors.affiliation: Gerontological Research Department, University of Ancona, Italy.
authors.forename: A R
authors.initials: AR
authors.lastname: Bonfigli
authors.forename: C
authors.initials: C
authors.lastname: Pieri
authors.forename: S
authors.initials: S
authors.lastname: Manfrini
authors.forename: I
authors.initials: I
authors.lastname: Testa
authors.forename: C
authors.initials: C
authors.lastname: Sirolla
authors.forename: R
authors.initials: R
authors.lastname: Ricciotti
authors.forename: M
authors.initials: M
authors.lastname: Marra
authors.forename: P
authors.initials: P
authors.lastname: Compagnucci
authors.forename: R
authors.initials: R
authors.lastname: Testa
mesh_terms: D000368:Aged; D000975:Antioxidants / Q000008:administration & dosage / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000517:prevention & control; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000096:biosynthesis / Q000097:blood*; D014810:Vitamin E / Q000008:administration & dosage* / Q000097:blood / Q000627:therapeutic use
chemical_list: D000975:Antioxidants; D017395:Plasminogen Activator Inhibitor 1; D014810:Vitamin E