Taq1b Polymorphism of Cholesteryl Ester Transfer Protein (Cetp) and Its Effects on the Serum Lipid Levels in Metabolic Syndrome Patients Publisher Pubmed



Maroufi NF¹ ; Farzaneh K² ; Alibabrdel M³ ; Zarei L³ ; Cheraghi O⁴ ; Soltani S⁴ ; Montazersaheb S⁵ ; Akbarzadeh M⁵ ; Nouri M⁵ Show Affiliations
Source: Biochemical Genetics Published:2016

Abstract

The metabolic syndrome (MetS) is one of the most important risk factors for type 2 diabetes and cardiovascular disease. This syndrome is characterized by abdominal obesity, hypertension, insulin resistance, and dyslipidemia. The plasma origin of Cholesteryl ester transfer protein (CETP) is responsible for transferring cholesterol esters from high-density lipoprotein particles to apolipoprotein B containing lipoproteins compartment. We conducted this study to investigate the association between CETP gene Taq1B (rs708272) polymorphism in the metabolic syndrome among Iranian subjects. A sample size of 200 patients diagnosed with MetS together with 200 healthy donors as control were enrolled in this study. The investigation of polymorphism was performed by the use of polymerase chain reaction and restriction fragment length polymorphism analysis. To determine the relationship between polymorphism and lipid profile, we measured lipids and CETP concentration in metabolic syndrome and control subjects. Genotype distribution and allelic frequencies of polymorphism were determined and compared in both groups. Our findings showed that all clinical and biochemical characteristics in patients differed from the control group. The results showed that genotype and allele frequency of the Taq1B polymorphism was not significantly different between two groups. Instinctively, CETP was significantly higher in metabolic syndrome (1.64 ± 0.32 µg/ml) than in control (1.53 ± 0.34 µg/ml). A low level of CETP was found in blood of B2B2 typified genotype. In spite of Taq1B polymorphism on ester transfer protein concentration, no direct correlation was found between this polymorphism and metabolic syndrome. © 2016, Springer Science+Business Media New York.