title: Postprandial thrombin activatable fibrinolysis inhibitor and markers of endothelial dysfunction in type 2 diabetic patients.
abstract: The aim of this study was to assess postprandial changes in thrombin activatable fibrinolysis inhibitor (TAFI) antigen, a thrombin-dependent fibrinolysis inhibitor with anti-inflammatory properties, and soluble markers of endothelial dysfunction in normotriglyceridemic type 2 diabetic patients. Fasting and postprandial TAFI antigen, thrombomodulin, tissue factor pathway inhibitor (TFPI), and plasminogen activator inhibitor 1 were assessed in 12 normotriglyceridemic type 2 diabetic patients treated with diet (hemoglobin A1c, 6.80% +/- 0.67%) and 14 controls. Fasting low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, free fatty acids and apolipoprotein B, and fasting and postprandial triglyceride, glucose, and insulin were also measured. Fasting TAFI was higher in the control group (102% +/- 16.9% vs 72.9% +/- 15.9%; P < .0005) and was inversely correlated with glycemic control. It decreased 4 hours after the meal (31.8% reduction [P < .005] for controls and 12.6% [P < .05] for diabetic patients) and returned to fasting levels after 8 hours. This decrement was correlated with fasting TAFI, glucose and hemoglobin A1c, and the area under the curve of glucose. Thrombomodulin, TFPI, and plasminogen activator inhibitor 1 were similar in both groups, with thrombomodulin and TFPI showing a transient postprandial increase. A fat-rich meal produces a transient increase in markers of endothelial dysfunction and a temporary reduction in TAFI, an anti-inflammatory molecule whose concentration is low in type 2 diabetes mellitus.
authors.affiliation: Endocrinology Department, Hospital Sant Pau. S Antoni M Claret 167, 08025 Barcelona, Spain. mrigla@santpau.es
authors.forename: Mercedes
authors.initials: M
authors.lastname: Rigla
authors.forename: Ana Maria
authors.initials: AM
authors.lastname: Wägner
authors.forename: Montserrat
authors.initials: M
authors.lastname: Borrell
authors.forename: José
authors.initials: J
authors.lastname: Mateo
authors.forename: Jordi
authors.initials: J
authors.lastname: Foncuberta
authors.forename: Alberto
authors.initials: A
authors.lastname: de Leiva
authors.forename: Jordi
authors.initials: J
authors.lastname: Ordóñez-Llanos
authors.forename: A
authors.initials: A
authors.lastname: Pérez
mesh_terms: D001055:Apolipoproteins B / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D025901:Carboxypeptidase B2 / Q000097:blood*; D002784:Cholesterol / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000502:physiology*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D019518:Postprandial Period / Q000502:physiology*; D018180:Thrombomodulin / Q000097:blood; D014280:Triglycerides / Q000097:blood
chemical_list: D001055:Apolipoproteins B; D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D008074:Lipoproteins; D017395:Plasminogen Activator Inhibitor 1; D018180:Thrombomodulin; D014280:Triglycerides; C051928:lipoprotein-associated coagulation inhibitor; D002784:Cholesterol; D025901:Carboxypeptidase B2