Abstract
The APOA1/C3/A4/A5 gene cluster encodes important regulators of fasting lipids, but the majority of lipid metabolism takes place in the postprandial state and knowledge about gene regulation in this state is scarce. With the aim of characterizing possible regulators of lipid metabolism, we studied the effects of nine single nucleotide polymorphisms (SNPs) during postprandial lipid metabolism. Eighty-eight healthy young men were genotyped for APOA1 -2630 (rs613808), APOA1 -2803 (rs2727784), APOA1 -3012 (rs11216158), APOC3 -640 (rs2542052), APOC3 -2886 (rs2542051), APOC3 G34G (rs4520), APOA4 N147S (rs5104), APOA4 T29T (rs5092), and A4A5_inter (rs1263177) and were fed a saturated fatty acid-rich meal (1g fat/kg of weight with 60% fat, 15% protein and 25% carbohydrate). Serial blood samples were extracted for 11 h after the meal. Total cholesterol and fractions [HDL-cholesterol, LDL-cholesterol, trifacylglycerols (TGs) in plasma, TG-rich lipoproteins (TRLs) (large TRLs and small TRLs), apolipoprotein A-I and apolipoprotein B] were determined. APOA1 -2803 homozygotes for the minor allele and A4A5_inter carriers showed a limited degree of postprandial lipemia. Carriers of the rare alleles of APOA4 N147S and APOA4 T29T had lower APOA1 plasma concentration during this state. APOC3 -640 was associated with altered TG kinetics but not its magnitude. We have identified new associations between SNPs in the APOA1/C3/A4/A5 gene cluster and altered postprandial lipid metabolism.
Highlights
The Apolipoprotein A1 (APOA1)/C3/A4/A5 gene cluster encodes important regulators of fasting lipids, but the majority of lipid metabolism takes place in the postprandial state and knowledge about gene regulation in this state is scarce
Diets rich in monounsaturated fat provoke a faster postprandial TGrich lipoprotein (TRL) clearance when compared with diets pronounced in saturated fat, shortening the lipemia, which may be mediated by postprandial apolipoproteins [5] and TRL metabolism [6]
We selected the single nucleotide polymorphism (SNP) analyzed in the present study on the basis of their localization within the APOA1/ C3/A4/A5 cluster, previous studies on fasting lipids, and/or computational analysis of putative function
Summary
The APOA1/C3/A4/A5 gene cluster encodes important regulators of fasting lipids, but the majority of lipid metabolism takes place in the postprandial state and knowledge about gene regulation in this state is scarce. We have identified new associations between SNPs in the APOA1/ C3/A4/A5 gene cluster and altered postprandial lipid metabolism.—Delgado-Lista, J., F. Effects of variations in the APOA1/C3/A4/A5 gene cluster on different parameters of postprandial lipid metabolism in healthy young men. Diet is the main external determinant of postprandial lipemia magnitude. It has been stated that carbohydrate intake increases the plasma concentration of postprandial lipid particles [triacylglycerols (TGs) and VLDL] when replacing fat in the diet [2, 3]. Diets rich in monounsaturated fat provoke a faster postprandial TGrich lipoprotein (TRL) clearance when compared with diets pronounced in saturated fat, shortening the lipemia, which may be mediated by postprandial apolipoproteins [5] and TRL metabolism [6].
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