کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1965475 | 1538667 | 2014 | 6 صفحه PDF | دانلود رایگان |

• Gender specific association of APOA1 gene with MetS traits risk.
• 75G > A polymorphism influences serum HDL-C levels among Turkish adults.
• APOA1 − 75GA genotype is independently related to atherogenic dyslipidemia.
• Male − 75A allele carriers had significantly higher diastolic BP.
• Gender-modulated associations suggest novel gene-gender-environmental interactions.
BackgroundVariations in the apolipoprotein A-1 (APOA1) gene, a determinant of plasma high-density lipoprotein cholesterol (HDL-C) and apoA-I levels, may contribute to cardiovascular diseases. We evaluated the effects of a promoter polymorphism (− 75G > A) in the APOA1 gene on metabolic syndrome (MetS) components in a Turkish population sample.MethodsRandomly selected 1515 Turkish adults (age 49.9 ± 11.8 years, 785 females) were genotyped for − 75G > A polymorphism using hybridization probes in Real-Time PCR LC480 device. MetS and atherogenic dyslipidemia were defined using the criteria of ATP III.ResultsThe − 75AA genotype prevailed in 3.9% of men and 2.4% of women, and was independently associated with significantly higher HDL-C concentrations. Independent associations with the − 75GA genotype existed only in men: higher diastolic and systolic blood pressure (BP) levels (p < 0.05) were observed in male − 75GA heterozygotes. Logistic regression revealed that the GA genotype confers elevated risk for atherogenic dyslipidemia (OR = 1.57, 95% Cl 1.06–2.3) after adjustment for associated risk factors. Independent associations with atherogenic dyslipidemia or elevated BP did not emerge in women.ConclusionAPOA1 − 75G > A polymorphism is independently related to HDL-C concentrations. Independent associations of the − 75GA genotype with elevated BP and atherogenic dyslipidemia were confined to men. These gender-modulated associations suggest novel gene–gender–environmental interactions.
Journal: Clinica Chimica Acta - Volume 431, 20 April 2014, Pages 244–249