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Research Department of Human Nutrition and Center for Advanced Food Studies; The Royal Veterinary and Agricultural University, Frederiksberg, Denmark and * Human Nutrition Unit Department of Biochemistry, University of Sydney, New South Wales 2006, Australia
2To whom correspondence should be addressed. E-mail: Tine.Tholstrup{at}fhe.kvl.dk.
Lipoprotein(a) [Lp(a)] is considered a risk factor for coronary heart disease. Our aim was to investigate the effect of individual fatty acids on postprandial plasma Lp(a) and its association with lipemia and tissue plasminogen activator (t-PA). Five test fats dominated by (approximately 43% g/kg) stearic (S), palmitic (P), oleic, C18:1 trans (T), or linoleic acid were produced by interesterification. Sixteen young healthy men were served the individual test fats incorporated into meals (1g fat/kg body wt) after a 12-h fast in random order on different days, separated by 3-wk washout periods. Blood samples were drawn before and 2, 4, 6, and 8 h after eating. There was a pronounced increase in Lp(a) concentrations after intake of the test meals, and the test fats resulted in a difference in Lp(a) response (P < 0.001; diet x time interaction). However, T fat did not change Lp(a) during the time course studied. T fat resulted in less area under the plasma Lp(a) concentration curve compared to S and P fat (P
0.003). Test fat with saturated fatty acids resulted in the highest Lp(a) and lowest plasma triacylglycerol (TAG) response, with the reversed situation for T fat. There was no association between Lp(a) and t-PA. In conclusion, intake of meals high in individual dietary fatty acids increased postprandial plasma Lp(a) differently. There seems to be a complex regulatory role of plasma TAG on nonfasting plasma Lp(a) concentrations.
KEY WORDS: lipoprotein(a) postprandial lipemia stearic acid trans fatty acid oleic acid
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