Abstract
The cholesteryl ester transfer protein (CETP) gene encodes a hydrophobic glycoprotein that plays a crucial role in the reverse transport of cholesterol. The aim of the present study was to determine whether CETP polymorphisms (rs1532624, rs247616 and rs708272) are associated with coronary artery disease (CAD) in a Polish population. Serum lipid levels and single nucleotide polymorphisms of CETP genes were determined in 494 subjects: 248 patients with premature CAD and 246 blood donors as controls. Selected polymorphisms were examined using TaqMan PCR analysis. We found that CAD risk was significantly higher for CC homozygotes and C allele carriers of the rs247616 polymorphism than for carriers with the T allele (OR 1.89, 95% CI 1.29–2.76, p = 0.001 and OR 1.51, 95% CI 1.14–1.99, p = 0.003) and likewise for the CC genotype of the rs1532624 polymorphism than for those with the A allele (OR 1.59, 95% CI 1.05–2.40, p = 0.026). Moreover, T allele carriers of the rs708272 polymorphism had significantly higher total cholesterol levels compared to CC homozygotes (p < 0.05) in the healthy controls. We also observed an allelic pattern, C(rs2477616)C(rs708272)C(rs1532624), which increased susceptibility to CAD by 43% (OR = 1.43, 95% CI 1.10–1.85, p = 0.006). In conclusion, the rs247616 and rs1532624 polymorphisms of CETP may modulate the risk of CAD in Polish population.
Highlights
Coronary artery disease is currently one of the main causes of morbidity and mortality worldwide
Cholesterol esters are transferred from high-density lipoprotein (HDL) to low-density lipoprotein (LDL), tri‐ glyceride-rich lipoproteins (TRL) chylomicrons, and very low-density lipoprotein (VLDL), while triacylglycerols are transferred from TRL to LDL and HDL [7]
Numer‐ ous studies have shown that high gene activity may result in reduced high-density lipoprotein cholesterol (HDL-C) levels [8,9,10,11] and, the development of ath‐ erosclerotic lesions and increased risk of coronary artery disease (CAD) [12, 13]
Summary
Coronary artery disease is currently one of the main causes of morbidity and mortality worldwide. Disorders of the lipid metabolism are crucial risk factors predispos‐ ing to the development of cardiovascular diseases [1]. Numer‐ ous studies have shown that high gene activity may result in reduced high-density lipoprotein cholesterol (HDL-C) levels [8,9,10,11] and, the development of ath‐ erosclerotic lesions and increased risk of coronary artery disease (CAD) [12, 13]. Not all studies confirm this dependency [14, 15], and combination therapy with statins and fibrates or CETP inhibitors has not produced the expected results in the reduction of cardiovascular events, despite elevated HDL-C levels [16,17,18]. How‐ ever, other authors suggest a lack of association [22,23,24]
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