METHODS: Using 3 d of dietary records, FA intakes of 333 recruited patients were calculated using a food database built from laboratory analyses of commonly consumed Malaysian foods. Plasma triacylglycerol (TG) and erythrocyte FAs were determined by gas chromatography.
RESULTS: High dietary saturated fatty acid (SFA) and monounsaturated fatty acid (MUFA) consumption trends were observed. Patients on HD also reported low dietary ω-3 and ω-6 polyunsaturated fatty acid (PUFA) consumptions and low levels of TG and erythrocyte FAs. TG and dietary FAs were significantly associated respective to total PUFA, total ω-6 PUFA, 18:2 ω-6, total ω-3 PUFA, 18:3 ω-3, 22:6 ω-3, and trans 18:2 isomers (P < 0.05). Contrarily, only dietary total ω-3 PUFA and 22:6 ω-3 were significantly associated with erythrocyte FAs (P < 0.01). The highest tertile of fish and shellfish consumption reflected a significantly higher proportion of TG 22:6 ω-3. Dietary SFAs were directly associated with TG and erythrocyte MUFA, whereas dietary PUFAs were not.
CONCLUSION: TG and erythrocyte FAs serve as biomarkers of dietary PUFA intake in patients on HD. Elevation of circulating MUFA may be attributed to inadequate intake of PUFAs.
METHODS: This 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.
RESULTS: Plasma 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 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