title: Relationship between plasma plasminogen activator inhibitor-1 activity and VLDL triglyceride concentration, insulin levels and insulin sensitivity: studies in randomly selected normo- and hypertriglyceridaemic men.
abstract: Impaired fibrinolytic function secondary to elevated plasma plasminogen activator inhibitor-1 activity, hypertriglyceridaemia and hyperinsulinaemia are frequent findings in patients with coronary heart disease. It has been debated whether VLDL or insulin is the major regulator of plasma plasminogen activator inhibitor-1 activity. This study examines the relationships between plasma plasminogen activator inhibitor-1 activity and VLDL triglyceride concentration, fasting and post-oral glucose load insulin levels and insulin sensitivity, as estimated by the minimal model method. Subjects studied were randomly selected hypertriglyceridaemic (n = 65) and age-matched normotriglyceridaemic (n = 61) men, aged 40-50 years, recruited in a population survey. Plasma plasminogen activator inhibitor-1 activity was higher in the hypertriglyceridaemic than in the normotriglyceridaemic group (21 +/- 14 vs 10 +/- 8 mU/l; p < 0.01). The hypertriglyceridaemic group had higher serum insulin, basal as well as 2 h after intake of the oral glucose load, and a lower insulin sensitivity index. In univariate analysis, plasma plasminogen activator inhibitor-1 activity correlated positively with VLDL triglycerides in both the hyper- and normotriglyceridaemic groups (r = 0.43 r = 0.60, respectively) and negatively with the insulin sensitivity index (r = -0.35 r = -0.44, respectively). In multivariate analysis, VLDL triglyceride levels were found to be independently related to plasma plasminogen activator inhibitor-1 activity in both groups, whereas insulin sensitivity/serum insulin levels were not. An unexpected finding was that the serum activity of the enzyme gamma glutamyl transpeptidase appeared to influence the relationships for plasma plasminogen activator inhibitor-1 in the hypertriglyceridaemic group.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: King Gustaf V Research Institute, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden.
authors.forename: A
authors.initials: A
authors.lastname: Asplund-Carlson
authors.forename: A
authors.initials: A
authors.lastname: Hamsten
authors.forename: B
authors.initials: B
authors.lastname: Wiman
authors.forename: L A
authors.initials: LA
authors.lastname: Carlson
mesh_terms: D000328:Adult; D000428:Alcohol Drinking; D000704:Analysis of Variance; D000886:Anthropometry; D001835:Body Weight; D005951:Glucose Tolerance Test; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood*; D007328:Insulin / Q000097:blood*; D008019:Life Style; D008079:Lipoproteins, VLDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D012016:Reference Values; D012907:Smoking; D014280:Triglycerides / Q000097:blood*; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D007328:Insulin; D008079:Lipoproteins, VLDL; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides; C030106:very low density lipoprotein triglyceride; D005723:gamma-Glutamyltransferase