Palm oil-enriched diets reduced plasma Lp(a) in volunteers with abnormally high concentrations: involvement of decreased triglyceride-rich APO(a)

• Published in: Nutrition research (New York, N.Y.) N.Y.), 2002, Vol.22 (7), p.769-784
• Main Authors: Mutalib, M.S.A, Khaza’ai, H, Peace, H, Whiting, P, Wahle, K.W.J
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; blood; CE-Lp(a); cholesterol; dietary fat; experimental diets; fat intake; Feeding. Feeding behavior; fish oils; Fundamental and applied biological sciences. Psychology; Heart disease; Lipoprotein(a); normal values; Palm oil; palm oils; Postprandial; risk; TRP-apo(a); Tryglyceride; Vertebrates: anatomy and physiology, studies on body, several organs or systems; volunteers
• ISSN: 0271-5317; 1879-0739
• DOI: 10.1016/S0271-5317(02)00379-2

Although plasma Lp(a) concentration is thought to be genectically determined, several studies have shown that certain dietary oils such as palm and fish oils can reduce its concentration in plasma. The present study, therefore, was conducted to identify possible mechanism whereby these dietary fat modifications lowered plasma Lp(a) concentration. Eleven healthy subjects with plasma Lp(a) concentrations >30 mg/dl received a palm oil diet (65% total fat intake) for 4 weeks. Blood samples were taken 12 hours pre-prandially and 4 hours post-prandially, for baseline assays prior to consumption of experimental diets, and at 2 week intervals thereafter. Individuals were therefore deemed to be their own controls. Pre- and post-prandial total Lp(a) decreased by 10% ( P < 0.001) and 7% respectively at the end of the study compared to baseline values. Plasma samples were separated into triglyceride-rich particle-(TRP)-apo(a) and cholesterol ester (CE) Lp(a) fractions by ultra-centrifugation. Individual contributions to the significant decrease in pre-prandial total Lp(a) concentrations were determined. Post-prandial TRP-apo(a) concentrations at week 4 were decreased compared to baseline (week 0). 10 subjects showed decreases of 0.25 mg/dl to 3.5 mg/dl. At week 0, post-prandial CE-Lp(a) concentrations were higher than pre-prandial levels. In contrast, at week 4 the post-prandial CE-Lp(a) levels were lower compared to respective pre-prandial levels. Increased pre-prandial concentrations of 0.6 to 12.5 mg/dl in 7 of the subjects and decreases in post-prandial concentrations of 0.1 to 27 mg/dl in 8 of the subjects at week 4 compared to week 0 were similar to changes observed in plasma TRP-apo(a) concentrations. This suggested that both fractions (TRP-apo(a) and CE-Lp(a)), contributed to the observed changes in total Lp(a) concentrations. Reductions in post-prandial total Lp(a) concentrations were most likely due to changes in post-prandial TRP-apo(a). Reciprocal changes in apo(a) between the TRP- and CE-Lp(a) fractions, particularly during the post-prandial phase, were also determined. No consistent relationships between the apo(a) content in the two fractions were observed but the mean ratio of TRP-apo(a) to CE-Lp(a) fraction was 1:50 in the pre-prandial states and ∼1:25 in the post-prandial states suggesting an increased preference of post-prandial apo(a) for TRP. The significance of these changes to total plasma Lp(a) concentration and to vascular disease risk is uncl