Abstract
BackgroundPostprandial lipemia (PL) contributes to coronary artery disease. The fatty acid composition of dietary fats is potentially a modifiable factor in modulating PL response.MethodsThis human postprandial study evaluated 3 edible fat blends with differing polyunsaturated to saturated fatty acids (P/S) ratios (POL = 0.27, AHA = 1.00, PCAN = 1.32). A cross-over design included mildly hypercholestrolemic subjects (9 men and 6 women) preconditioned on test diets fats at 31% energy for 7 days prior to the postprandial challenge on the 8th day with 50 g test fat. Plasma lipids and lipoproteins were monitored at 0, 1.5, 3.5, 5.5 and 7 hr.ResultsPlasma triacylglycerol (TAG) concentrations in response to POL, AHA or PCAN meals were not significant for time x test meal interactions (P > 0.05) despite an observed trend (POL > AHA > PCAN). TAG area-under-the-curve (AUC) increased by 22.58% after POL and 7.63% after PCAN compared to AHA treatments (P > 0.05). Plasma total cholesterol (TC) response was not significant between meals (P > 0.05). Varying P/S ratios of test meals significantly altered prandial high density lipoprotein-cholesterol (HDL-C) concentrations (P < 0.001) which increased with decreasing P/S ratio (POL > AHA > PCAN). Paired comparisons was significant between POL vs PCAN (P = 0.009) but not with AHA or between AHA vs PCAN (P > 0.05). A significantly higher HDL-C AUC for POL vs AHA (P = 0.015) and PCAN (P = 0.001) was observed. HDL-C AUC increased for POL by 25.38% and 16.0% compared to PCAN and AHA respectively. Plasma low density lipoprotein-cholesterol (LDL-C) concentrations was significant (P = 0.005) between meals and significantly lowest after POL meal compared to PCAN (P = 0.004) and AHA (P > 0.05) but not between AHA vs PCAN (P > 0.05). AUC for LDL-C was not significant between diets (P > 0.05). Palmitic (C16:0), oleic (C18:1), linoleic (C18:2) and linolenic (C18:3) acids in TAGs and cholesteryl esters were significantly modulated by meal source (P < 0.05).ConclusionsP/S ratio of dietary fats significantly affected prandial HDL-C levels without affecting lipemia.
Highlights
Postprandial lipemia (PL) contributes to coronary artery disease
Prolonged circulation of triacylglycerol-rich lipoproteins (TRL) and suppression of high density lipoproteincholesterol (HDL-C) concentrations are independently linked to atherogenicity progression and early death in type 2 diabetes with similar associations observed in metabolic syndrome, obesity and hypertriglyceridemia [8,9]
Lipemic response and test fat clearance Based on postprandial plasma TAGs [Figure 1A], a higher degree of lipemia was observed with decreasing polyunsaturated to saturated fatty acids (P/S) ratio (POL > AHA > PCAN) the effect of time × meal treatment changes was not significant (P > 0.05)
Summary
Postprandial lipemia (PL) contributes to coronary artery disease. Plasma triacylglycerol (TAG) in the post-meal state mainly comprises triacylglycerol-rich lipoproteins (TRL) carried by chylomicrons [1]. Elevated TAG triggers a chain of metabolic reactions that may reduce high density lipoproteincholesterol (HDL-C), promote formation of small dense low density lipoprotein (LDL) particles and activate prothrombotic factor FVII [2,3,4]. The induction of endothelial dysfunction as well as a prothrombic state may contribute to cardiovascular dysfunction [5,6]. The post-meal state, its resulting postprandial lipemia and increased generation of TRL are recognized as modifiable cardiovascular disease (CVD) risk factors [7]. Prolonged circulation of TRL and suppression of HDL-C concentrations are independently linked to atherogenicity progression and early death in type 2 diabetes with similar associations observed in metabolic syndrome, obesity and hypertriglyceridemia [8,9]
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