Most studies on lipid lowering diets have focused on the total content of saturated, polyunsaturated and monounsaturated fatty acids. However, the distribution of these fatty acids on the triacylglycerol (TAG) molecule and the molecular TAG species generated by this stereospecificity are characteristic for various native dietary TAGs. Fat randomization or interesterification is a process involving the positional redistribution of fatty acids, which leads to the generation of new TAG molecular species. A comparison between native and randomized TAGs is the subject of this review with regards to the role of stereospecificity of fatty acids in metabolic processing and effects on fasting lipids and postprandial lipemia. The positioning of unsaturated versus saturated fatty acids in the sn-2 position of TAGs indicate differences in early metabolic processing and postprandial clearance, which may explain modulatory effects on atherogenecity and thrombogenecity. Both human and animal studies are discussed with implications for human health.

Background: Tocotrienols (T3) and tocopherols (T), both members of the natural vitamin E family have unique biological functions in humans. T3 are detected in circulating human plasma and lipoproteins, although at concentrations significantly lower than α-tocopherol (α-T). T3, especially α-T3 is known to be neuropotective at nanomolar concentrations and this study evaluated the postprandial fate of T3 and α-T in plasma and lipoproteins. Methods: Ten healthy volunteers (5 males and 5 females) were administered a single dose of vitamin E [526 mg palm tocotrienol-rich fraction (TRF) or 537 mg α-T] after 7-d pre-conditioning on a T3-free diet. Blood was sampled at baseline (fasted) and 2, 4, 5, 6, 8, and 24 h after supplementation. Concentrations of T and T3 isomers in plasma, triacylglycerol-rich particles (TRP), LDL, and HDL were measured at each postprandial interval. Results: After TRF supplementation, plasma α-T3 and γ-T3 peaked at 5 h (α-T3: 4.74 ± 1.69 μM; γ-T3: 2.73 ± 1.27 μM). δ-T3 peaked earlier at 4 h (0.53 ± 0.25 μM). In contrast, α-T peaked at 6 h (30.13 ± 2.91 μM) and 8 h (37.80 ± 3.59 μM) following supplementation with TRF and α-T, respectively. α-T was the major vitamin E isomer detected in plasma, TRP, LDL, and HDL even after supplementation with TRF (composed of 70% T3). No T3 were detected during fasted states. T3 are detected postprandially only after TRF supplementation and concentrations were significantly lower than α-T. Conclusions: Bio-discrimination between vitamin E isomers in humans reduces the rate of T3 absorption and affects their incorporation into lipoproteins. Although low absorption of T3 into circulation may impact some of their physiological functions in humans, T3 have biological functions well below concentration noted in this study.

We conducted this cross-sectional population study with a healthy multi-ethnic urban population (n = 577) in Malaysia, combining nutritional assessments with cardiometabolic biomarkers defined by lipid, atherogenic lipoproteins, inflammation and insulin resistance. We found diametrically opposing associations of carbohydrate (246·6 ± 57·7 g, 54·3 ± 6·5%-TEI) and fat (total = 64·5 ± 19·8 g, 31·6 ± 5·5%-TEI; saturated fat = 14·1 ± 2·7%-TEI) intakes as regards waist circumference, HDL-C, blood pressure, glucose, insulin and HOMA2-IR as well as the large-LDL and large-HDL lipoprotein particles. Diets were then differentiated into either low fat (LF, <30% TEI or 35% TEI or >70 g) and low carbohydrate (LC, 285 g) which yielded LFLC, LFHC, HFLC and HFHC groupings. Cardiometabolic biomarkers were not significantly different (P > 0.05) between LFLC and HFLC groups. LFLC had significantly higher large-LDL particle concentrations compared to HFHC. HOMA-IR2 was significantly higher with HFHC (1·91 ± 1·85, P < 0·001) versus other fat-carbohydrate combinations (LFLC = 1·34 ± 1·07, HFLC = 1·41 ± 1·07; LFHC = 1·31 ± 0·93). After co-variate adjustment, odds of having HOMA2-IR >1.7 in the HFHC group was 2.43 (95% CI: 1·03, 5·72) times more compared to LFLC while odds of having large-LDL <450 nmol/L in the HFHC group was 1.91 (95% CI: 1·06, 3·44) more compared to latter group. Our data suggests that a HFHC dietary combination in Malaysian adults is associated with significant impact on lipoprotein particles and insulin resistance.

Objective: Saturated fats increase total cholesterol (TC) and low density lipoprotein-cholesterol (LDL-C) and are linked to coronary artery disease risk. The effect of variance in chain length of saturated fatty acids (SFA) on coronary artery disease in human postprandial lipemia is not well elucidated. Methods: A total of 20 healthy volunteers were challenged with 3 test meals, similar in fat content (∼31% en) but varying in saturated SFA content and polyunsaturated/saturated fatty acid ratios (P/S). The 3 meals were lauric + myristic acid-rich (LM), P/S 0.19; palmitic acid-rich (POL), P/S 0.31; and stearic acid-rich (STE), P/S 0.22. Blood was sampled at fasted baseline and 2, 4, 5, 6, and 8 hours. Plasma lipids (triacylglycerol [TAG]) and lipoproteins (TC, LDL-C, high density lipoprotein-cholesterol [HDL-C]) were evaluated. Results: Varying SFA in the test meal significantly impacted postprandial TAG response (p < 0.05). Plasma TAG peaked at 5 hours for STE, 4 hours for POL, and 2 hours for LM test meals. Area-under-the-curve (AUC) for plasma TAG was increased significantly after STE treatment (STE > LM by 32.2%, p = 0.003; STE > POL by 27.9%, p = 0.023) but was not significantly different between POL and LM (POL > LM by 6.0%, p > 0.05). At 2 hours, plasma HDL-C increased significantly after the LM and POL test meals compared with STE (p < 0.05). In comparison to the STE test meal, HDL-C AUC was elevated 14.0% (p = 0.005) and 7.6% (p = 0.023) by the LM and POL test meals, respectively. The TC response was also increased significantly by LM compared with both POL and STE test meals (p < 0.05). Conclusions: Chain length of saturates clearly mediated postmeal plasma TAG and HDL-C changes.

Mayonnaise is used widely in contemporary human diet with widespread use as a salad dressing or spread on breads. Vegetable oils used in its formulation may be a rich source of ω-6 PUFAs and the higher-PUFA content of mayonnaise may be beneficial in mediating a hypocholesterolemic effect. This study, therefore, evaluated the functionality of mayonnaise on cardiometabolic risk within a regular human consumption scenario. Subjects underwent a randomized double-blind crossover trial, consuming diets supplemented with 20 g/day of either soybean oil-based mayonnaise (SB-mayo) or palm olein-based mayonnaise (PO-mayo) for 4 weeks each with a 2-week wash-out period. The magnitude of changes for metabolic outcomes between dietary treatments was compared with PO-mayo serving as the control. The data was analyzed by ANCOVA using the GLM model. Analysis was adjusted for weight changes. Treatments resulted in significant reductions in TC (diff = −0.25 mmol/L; P = 0.001), LDL-C (diff = −0.17 mmol/L; P = 0.016) and HDL-C (diff = −0.12 mmol/L; P < 0.001) in SB-mayo compared to PO-mayo without affecting LDL-C:HDL-C ratio (P > 0.05). Lipoprotein particle change was significant with large LDL particles increasing after PO-mayo (diff = +63.2 nmol/L; P = 0.007) compared to SB-mayo but small LDL particles remained unaffected. Plasma glucose, apolipoproteins and oxidative stress markers remained unchanged. Daily use with 20 g of linoleic acid-rich SB-mayo elicited reductions in TC and LDL-C concentrations without significantly changing LDL-C:HDL-C ratio or small LDL particle distributions compared to the PO-mayo diet. This clinical trial was retrospectively registered with the National Medical Research Register, National Institute of Health, Ministry of Health Malaysia, (NMRR-15-40-24035; registered on 29/01/2015; https://www.nmrr.gov.my/fwbPage.jsp?fwbPageId=ResearchISRForm&fwbAction=Update&fwbStep=10&pk.researchID=24035&fwbVMenu=3&fwbResearchAction=Update ). Ethical approval was obtained from the National University of Malaysia’s Medical Ethics Committee (UKM 1.5.3.5/244/SPP/NN-054-2011, approved on 25/05/2011).

Postprandial lipemia (PL) contributes to coronary artery disease. The fatty acid composition of dietary fats is potentially a modifiable factor in modulating PL response.