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 ore important mechanisms in the pathogenesis of atherosclerosis. Methods and results: in a high fat meal group (n = Il). serum triglycerides and PMA-activated leukocyte O-2(-.) production were significantly (P < 0.005) increased from 146 69 mg/dl and 4.09 +/- 0.93 nmol/10(6) cells/min preprandially to 198 +/- 88 mg/dl and 5.49 +/- 1.19 nmol/10(6) cells:min. respectively. 2 h after eating a high-fat meal. The Row-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 rating a high-fat meal (P < 0.005). However. following a low-fat meal (n = 9). there were no significant changes in triglycerides, leukocyte O-2(-.) 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 O-2(-.) production, which in turn were correlated negatively (r = -0.783. 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. <(c)> 2001 Elsevier Science Ireland Ltd. All rights reserved.