Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress

Aims: it appears that hypertriglyceridemia (HTG) is a risk factor of atherosclerosis as demonstrated by recent studies. In this study, we analyzed the effects of acute HTG on endothelial function and oxidative stress, which are important mechanisms in the pathogenesis of atherosclerosis. Methods and results: in a high fat meal group (n=11), serum triglycerides and PMA-activated leukocyte O2−√ production were significantly (P<0.005) increased from 146±69 mg/dl and 4.09±0.93 nmol/106 cells/min preprandially to 198±88 mg/dl and 5.49±1.19 nmol/106 cells/min, respectively, 2 h after eating a high-fat meal. The flow-mediated endothelium-dependent brachial artery dilation (FMD; high-resolution ultrasound) was decreased from 13.7±3.3% preprandially to 8.2±3.7%, 2 h after eating a high-fat meal (P<0.005). However, following a low-fat meal (n=9), there were no significant changes in triglycerides, leukocyte O2−√ production and FMD. Changes of serum triglycerides were correlated negatively (r=−0.650, P<0.005) with changes of FMD, but were correlated positively (r=0.798, P<0.001) with changes of leukocyte O2−√ production, which — in turn — were correlated negatively (r=−0.784, P<0.001) with changes of FMD in all study subjects (mean age: 56 years, n=20). Conclusions: this study suggests that acute HTG causes endothelial dysfunction via enhanced oxidant stress and this may pave the way for the development of atherosclerosis under chronic conditions.