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The Influence of Lipoprotein Lipase Gene Variation on Postprandial Lipoprotein Metabolism

Lipids and Atherosclerosis Research Unit (J.L.-M., G.C., P.G., C.M., E.P., P.P.-M., F.J.F., F.P.-J.), Reina Sofía University Hospital, 14004 Córdoba. Spain; and Nutrition and Genomics Laboratory (J.M.O.), Tufts University, Boston, Massachusetts 02111

Address all correspondence and requests for reprints to: Francisco Pérez Jiménez, Unidad de Lípidos y Arteriosclerosis, Hospital Universitario Reina Sofía, Avda Menéndez Pidal, s/n. 14004 Córdoba, Spain. E-mail: md1pejif{at}uco.es.

Lipoprotein lipase (LPL) is one of the key enzymes in the metabolism of triacylglycerol-rich lipoproteins (TRL). We evaluated whether the association of LPL HindIII (H1/H2) and Serine447-Stop (S447X) polymorphisms may explain the interindividual variability observed during postprandial lipemia. Fifty-one healthy male volunteers (26 with the H2S447 genotype, 15 with the H1X447 genotype, and 10 with the H1S447 genotype) were subjected to a vitamin A-fat load test consisting of 1 g fat/kg body weight and 60,000 IU vitamin A. Blood was drawn every hour until the 6th hour and every 2 h and 30 min until the 11th hour. Data revealed that subjects that are homozygous for the H2 allele (H2H2) showed a higher postprandial response for small TRL, retinyl palmitate (RP), large TRL-RP, large TRL-B48, and small TRL-B48 levels. Furthermore, in the case of the S447X polymorphism, 447Ter carriers had a lower postprandial response for small TRL-RP, large TRL-B48, and small TRL-RP. Subjects with the LPL H2S447 genotype had higher plasma triacylglycerol, large TRL-triacylglycerol, large TRL-RP, small TRL-RP, and large TRL-B48 (P < 0.037) than H1X447 subjects. The modifications observed in postprandial lipoprotein metabolism in young normolipemic males with LPL polymorphism could be involved in the lower risk of coronary artery disease associated with the H1X447 genotype.

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