Abstract

The aim of the present study was to determine if there is an association between the single nucleotide polymorphisms (SNPs) of the lipoprotein lipase (LPL) and apolipoprotein E (apo E) genes and the serum lipid profile in pregnancy and puerperium. Non-diabetic women of European descent in the third semester of pregnancy (N = 120) were selected. Those with diseases or other condition that could modify their lipid profile were excluded from the study (N = 32). Serum lipids were measured by routine laboratory procedures and genomic DNA was extracted by a salting out method. LPL (PvuII and HindIII) and apo E (HhaI) SNPs were detected by the polymerase chain reaction and restriction fragment length polymorphism. Categorical and continuous variables were compared by the chi-square test and Student t-test or ANOVA, respectively. Women carrying the LPL P1P1 genotype had higher serum LDL cholesterol (N = 21; 155 +/- 45 mg/dL) than women carrying the P1P2/P2P2 genotypes (N = 67; 133 +/- 45 mg/dL; P = 0.032). During the puerperium period, serum levels of triglycerides and VLDL cholesterol were significantly reduced in women carrying the P1P1 (73%, P = 0.006) and P1P2 (51%, P = 0.002) genotypes but not in women carrying the P2P2 genotype (23%, P > 0.05). On the other hand, serum concentrations of lipids did not differ between the LPL HindIII and apo E genotypes during pregnancy and after delivery. We conclude that LPL PvuII SNP is associated with variations in serum lipids during pregnancy and the puerperal period in non-diabetic women.

Highlights

  • Lipoprotein lipase (LPL) is a glycoprotein synthesized by several tissues and cell types, including adipose, cardiac and skeletal tissues [1]

  • The aim of the present study was to determine if there is an association between the single nucleotide polymorphisms (SNPs) of the lipoprotein lipase (LPL) and apolipoprotein E genes and the serum lipid profile in pregnancy and puerperium

  • Serum levels of triglycerides and very low-density lipoproteins (VLDL) cholesterol were significantly reduced in women carrying the P1P1 (73%, P = 0.006) and P1P2 (51%, P = 0.002) genotypes but not in women carrying the P2P2 genotype (23%, P > 0.05)

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Summary

Introduction

Lipoprotein lipase (LPL) is a glycoprotein synthesized by several tissues and cell types, including adipose, cardiac and skeletal tissues [1]. LPL hydrolyzes triglycerides (TG) of circulating very low-density lipoproteins (VLDL) and chylomicrons, and generates fatty acids for storage in adipose tissue [1] During this process, these TGrich lipoproteins are converted to remnant particles which are removed from the circulation by interaction of apolipoproteins E (apo E) and B with specific receptors in the liver. The apo E gene has an HhaI single nucleotide polymorphism (SNP) that encodes three apo E isoforms named E2, E3 and E4 [8] These apo E isoforms interact with B/E and E receptors with different affinities that affect the removal of apo E-rich lipoproteins, VLDL and chylomicron remnants, and contribute to TG and cholesterol elevation in plasma [8]

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