In various groups of patients, plasminogen activator inhibitor (PAI),
plasma insulin and triglyceride level are closely associated all toget
her. To clarify this relationship we looked at PAI activity in patient
s with endogenous hypertriglyceridemia, 15 were obese (body mass index
(BMI) higher than 27, mean: 36.2), 9 had a strictly normal weight (BM
I lower than 25, mean: 22.8) and 11 had alcohol induced hypertriglycer
idemia. They were compared to 20 control subjects of normal weight and
with plasma triglyceride level lower than 1. 7 mmol/l and 11 hypercho
lesterolemic patients. Overall mean PAI levels in hypertriglyceridemic
patients were higher than in controls and hypercholesterolemic subjec
ts. Compared to controls (mean+/-SD PAI: 9.8+/-5.4 U/ml), both PAI act
ivity (30+/-12 U/ml p<0.05) and plasma insulin were elevated in obese
hypertriglyceridemic patients but not different from normal in the nor
mal weight hypertriglyceridemic patients (PAI activity 15.2+/-4.1 U/ml
ns). In alcoholic hypertriglyceridemic patients, PAI activity was ele
vated (21+/-9.7 U/ml p<0.05) but insulin was normal. In the whole seri
es PAI activity was weekly correlated with triglyceride level (r=0.295
p<0.05), but in strong positive relationship with insulin levels (r=0
.572 p<0.0001). These results suggest that in obese patients insulin r
esistance is the common cause of both hypertriglyceridemia and elevati
on of PAI activity. Other mechanisms have to be looked for in some con
ditions such as alcohol associated hypertriglyceridemia. Endogenous hy
pertriglyceridemia occurring in strictly normal weight subjects is not
accompanied by elevated PAI levels.