Evidence for a relationship between plasminogen activator inhibitor-1 and gamma glutamyl transferase

Abstract

Plasma plasminogen activator inhibitor-1 (PAI-1) levels are elevated in insulin-resistant obese subjects (1). However, the mechanisms responsible for such elevation are unknown. It has been shown that insulin increases PAI-1 synthesis by the human hepatoma cell line Hep G2 (2) and by freshly isolated human hepatocytes (3). Moreover, a recent study showed that PAI-1 synthesis in presence of insulin was markedly increased in Hep G2 cells down-regulated for insulin receptor (4); these results agree with those found in vivo in insulin-resistant subjects. On the other hand, it has recently been proposed that mild liver abnormalities and steatosis may be among the factors accounting for high plasma PAI-1 levels in hyperlipidemic subjects (5,6). Steatosis and hepatic abnormalities are also a common feature of obese subjects (7,8). Thus the purpose of this investigation was to determine whether plasma PAI-1 levels were correlated with hepatic enzymes in non-hypertriglyceridemic subjects with a wide range of body mass index (BMI) and levels of insulin resistance.