Lipoprotein lipase (LPL) is the key enzyme responsible for TRL triglyceride lipolysis within blood vessels; from VLDL or chylomicrons it generates TRL remnants that can be taken up by the liver or peripheral tissues and thus cleared from the circulation. Among more than 50 known polymorphisms, several common and important ones have been found in LPL gene, such as p.Asp9Asn or p.Asn291Ser, which both present a 4-6% frequency in Western populations, and SNP8393 in intron 8 (restriction site HindIII).
LPL activity can be somewhat reduced in subjects bearing the p.291S or the p.9N allele and these variants are associated with higher fasting triglycerides and lower HDL cholesterol levels (Gerdes et al., 1997; Senti et al., 2000). In heterozygote carriers of the p.291S variant, postprandial levels of large VLDL apoB48, triglycerides and retinyl palmitate were higher than in non-carriers (Mero et al., 1999). Regarding long-term dietary interventions, it has been reported that homologous carriers of the HindIII site had a significantly smaller change in mean total plasma cholesterol in response to diet than others (Humphries et al., 1996).
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