To our knowledge, the current research is the first time to investigate the effect of the n-6/n-3 PUFAs ratio on the postprandial lipid, glucose and insulin metabolism, inflammatory response and endothelial function in hypertriacylglycerolemia subjects, comparing them to normal controls. According to repeated–measures ANOVA, the postprandial response of lipid, glucose, insulin inflammation and endothelial function after high n-3 test meal were not significantly different from that after low n-3 test meal, but the postprandial lipid response was exaggerated in HTG subjects regardless of test meal, and low n-3 test meals strengthened the difference between HTG and HC groups.
Previous studies suggested that increasing consumption of n-3 PUFAs could improve lipid metabolism both in the fasting and postprandial states , however in our study, the postprandial lipid response was not different between the high and low n-3 test meals, suggesting that n-3 PUFA needs more than 8 hours to exert these beneficial effects and the fatty acids content of background diet maybe more effective than the type of fatty acids in test meal to influence the postprandial response . Furthermore, the pure fat test with high n-3 PUFAs also can not acutely improve postprandial lipid response in men with metabolic syndrome . Although differences in postprandial responses were not observed between the meals, the pattern of TG response was different in HTG group and HC group. The peak point of the blood TG concentration was 4 h postmeal after eating the high n-3 meals but 6 h after the low n-3 meal in HTG group. The prolonged elevation in TG concentration may reflect the prolonged either slower absorption or to increased lipolysis. Shah et al.  also pointed that test meals rich in DHA and EPA (the representative of n-3 PUFAs) may reduce the TG response, but the difference was not significant between DHA and EPA and linoleic acid (the representative of n-6 PUFAs). Given the TC, HDL, ApoA, ApoB is an acknowledge marker of lipid metabolism in the fasting state, in our research the concentration of these were also measured in postprandial samples. But all these markers did not show any marked change over time after meals (data not show), which is accordance with the previous studies [23, 24], suggesting that the postprandial rate of their catabolism and synthesis was slow. So measuring these markers will not add new information for postprandial response.
Subjects with fasting hypertriglyceridemia usually have elevated and prolonged postprandial lipid response . In the present study it is apparent that HTG subjects tended to have greater postprandial increase in TG levels relative to healthy controls, which is in good agreement with most studies [25–27]. Furthermore the difference in the magnitude of postprandial TG response was strengthened by low n-3 test meal. After both test meals maximal change and iAUC for TG was all higher in HTG group than HC group, the difference were significant after low n-3 test but not after high n-3 test. Hypertriglyceridemia subjects show slower clearance of glucose, larger insulin increases and more extravagant endothelial dysfunction . Although in our study the concentration of glucose, insulin, IL-6, TNFα and ET-1 at each time point was higher NO was lower in HTG group, but the maximal change and iAUC had no significant difference except for iAUC of insulin, IL-6 and diAUC of NO after low n-3 test meals.
Postprandial period is regarded as pro-inflammatory state, indicated by elevated levels of inflammatory proteins such as IL-6 and TNFα. There is evidence that n-3 fatty acids are anti-inflammatory, but n-6 fatty acids are pro-inflammatory [9, 29]. However our results suggest that the ratio of n-6 and n-3 in test meal does not acutely influence inflammatory status in HTC and HC subjects. The magnitude of the postprandial increase in plasma IL-6 and TNFα was similar after high n-3 and low n-3 meals in both groups. Earlier studies have demonstrated that IL-6 increases from morning to night irrespective of food intake [30–32]. So the increase of IL-6 levels in our research maybe confounded because of blood drawing procedure . Plasma TNFα concentration increased in parallel with plasma IL-6 concentration in current study, which could be partly explained by the elevation of the number of monocytes expressing TNFα within visceral adipose tissue [34, 35]. Other studies in obesity and diabetes men, TNFα concentrations were unchanged or decreased [36, 37]. Possible reasons for conflicting results could be the differences in population in study and composition of the test meal.
The postprandial state, characterized by elevations in TG, is a proinflammatory situation contributing to endothelial dysfunction that is considered the earliest stage of atherosclerotic . NO and ET-1 are major vasodilator and vasoconstrictor endothelium-derived substances respectively, and their role and reciprocal interactions in endothelial function have been extensively accepted. In our research postprandial endothelial function impaired with decreasing of NO and increasing of ET-1 after test meals, which are consistent with many previous studies [39, 40]. It is well known that intake of n-3 fatty acids is inversely associated with biomarkers of inflammation and endothelial activation [40, 41]. In our current research high n-3 test meal does not improve the postprandial endothelial disfunction in HTC and HC subjects. It is apparent that HTG subjects tended to have greater postprandial decrease in NO levels compared to healthy controls, which further proved that transient increase in TG increase the risk of atherosclerosis. The disordered postprandial metabolism of triglyceride-riched lipoproteins may play an atherogenic role by inducing endothelial dysfunction .