Neslihan Coban1, Altan Onat2, Filiz Guclu-Geyik3, Evrim Komurcu-Bayrak4, Gunay Can5, Nihan Erginel-Unaltuna6. 1. Department of Genetics, Institute for Experimental Medicine, Istanbul University, Istanbul, Turkey. Electronic address: neslihancoban@yahoo.com. 2. Department of Cardiology, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey. Electronic address: alt_onat@yahoo.com.tr. 3. Department of Genetics, Institute for Experimental Medicine, Istanbul University, Istanbul, Turkey. Electronic address: filiz.geyik@gmail.com. 4. Department of Genetics, Institute for Experimental Medicine, Istanbul University, Istanbul, Turkey. Electronic address: evrimbayrak@yahoo.com. 5. Cerrahpaşa Medical Faculty, Depatrment of Public Health, Istanbul University, Istanbul, Turkey. Electronic address: alpincan@yahoo.fr. 6. Department of Genetics, Institute for Experimental Medicine, Istanbul University, Istanbul, Turkey. Electronic address: nihanerginel@yahoo.com.
Abstract
BACKGROUND: Variations 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. METHODS: Randomly 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. RESULTS: The -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. CONCLUSION: APOA1 -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.
BACKGROUND: Variations 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. METHODS: Randomly 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. RESULTS: The -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. CONCLUSION:APOA1 -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.