Association of the CETP Taq1B and LIPG Thr111Ile Polymorphisms with Glycated Hemoglobin and Blood Lipids in Newly Diagnosed Hyperlipidemic Patients

Abstract Objective To examine the association of 2 common polymorphisms in high-density lipoprotein (HDL)-related genes, namely, cholesterol ester transfer protein CETP Taq1B (rs708272) and endothelial lipase LIPG Thr111Ile (rs2000813), with glycated hemoglobin (A1C), blood lipid levels and the risk...

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Veröffentlicht in:Canadian journal of diabetes 2016-12, Vol.40 (6), p.515-520
Hauptverfasser: Agapakis, Dimitrios, MD, Savopoulos, Christos, MD, PhD, Kypreos, Kyriakos E., PhD, Gbandi, Emma, MSc, PhD, Iliadis, Stavros, MSc, MD, PhD, Hatzitolios, Apostolos I., MD, PhD, Goulas, Antonis, MA, MD, PhD
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Sprache:eng
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Zusammenfassung:Abstract Objective To examine the association of 2 common polymorphisms in high-density lipoprotein (HDL)-related genes, namely, cholesterol ester transfer protein CETP Taq1B (rs708272) and endothelial lipase LIPG Thr111Ile (rs2000813), with glycated hemoglobin (A1C), blood lipid levels and the risk for type 2 diabetes in a group of hyperlipidemic patients from northern Greece. Methods We categorized 175 patients with hyperlipidemia into 2 subgroups according to the presence or absence of type 2 diabetes, defined as a recent diagnosis, A1C >6.5% and/or fasting glucose >126 mg/dL. Genotypes for the 2 polymorphisms studied were determined by polymerase chain reaction-restriction fragment length polymorphism. Both polymorphisms were analyzed by multivariate and univariate analyses of baseline A1C levels and plasma lipids. The genotype and allele frequencies of the 2 subgroups were compared. Results The CETP Taq1B polymorphism was associated with HDL-cholesterol (HDL-C) and A1C levels, but this association was affected by type 2 diabetes; the association with A1C levels was significant only in type 2 diabetes (p=0.005), whereas the association with HDL-C occurred only in the subgroup without type 2 diabetes (p
ISSN:1499-2671
2352-3840
DOI:10.1016/j.jcjd.2016.01.002