Mohsen Valizadeh1, Maliheh Aghasizadeh2, Mohsen Nemati3, Mohammad Hashemi4, Seyed Hamid Aghaee-Bakhtiari5, Reza Zare-Feyzabadi6, Habibollah Esmaily7, Hamideh Ghazizdaeh8, Reza Sahebi9, Najmeh Ahangari1, Gordon A Ferns10, Alireza Pasdar11, Majid Ghayour-Mobarhan12. 1. Department of Medical Genetics and Molecular Medicine, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 2. Cardiovascular Diseases Research School Center, Birjand University of Medical Sciences, Birjand, Iran; Student research Committee, Department of Molecular Medicine, Faculty of medicine, Birjand University of Medical Sciences, Birjand, Iran; International UNESCO Center for Health-Related Basic Sciences and Human Nutrition, Mashhad University of Medical Sciences, Mashhad, Iran. 3. Department of Nutrition, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 4. Medical Toxicology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. 5. Department of Biotechnology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran; Bioinformatics Research Group, Mashhad University of Medical Sciences, Mashhad, Iran. 6. Metabolic syndrome Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. 7. Social Determinants of Health Research Center, Mashhad University of Medical sciences, Mashhad, Iran. 8. International UNESCO Center for Health-Related Basic Sciences and Human Nutrition, Mashhad University of Medical Sciences, Mashhad, Iran; Student Research Committee, Mashhad University of Medical Sciences, Mashhad, Iran. 9. Metabolic syndrome Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Department of Molecular Medicine, School of Advanced Technologies, Shahrekord University of Medical Sciences, Shahrekord, Iran. 10. Brighton & Sussex Medical School, Division of Medical Education, Falmer, Brighton, Sussex, UK. 11. Department of Medical Genetics and Molecular Medicine, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran; Bioinformatics Research Group, Mashhad University of Medical Sciences, Mashhad, Iran; Division of Applied Medicine, Medical School, University of Aberdeen, Foresterhill, Aberdeen, UK. Electronic address: pasdara@mums.ac.ir. 12. Department of Nutrition, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran; Metabolic syndrome Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; International UNESCO Center for Health-Related Basic Sciences and Human Nutrition, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: ghayourm@mums.ac.ir.
Abstract
INTRODUCTION: Dyslipidemia is a known risk factor for cardiovascular disease and is partially determined by genetic variations in the genes involved in lipoprotein metabolism. Therefore, we aimed to assess the association between a polymorphism of the Fatty Acid Binding Protein1 (rs2241883) gene locus and dyslipidemia in an Iranian cohort. MATERIALS AND METHODS: This is a case-control study 2737 individuals were recruited (2203 subjects with dyslipidemia and 534 controls). Dyslipidemia was defined as total cholesterol≥200 mg/dl, or TG≥150 mg/dl, or LDL-C≥130 mg/dl, or HDL-C<40 mg/dl in males and <50 mg/dl in females. Serum lipid profile was determined using a Alcyon Abbott biochemical auto analyzer, USA. Genotyping was made through double amplification refractory mutation system polymerase chain reaction (ARMs PCR). RESULT: The frequency of TT, CT, CC genotypes of rs2241883 polymorphism of FABP1 gene were 65.5, 33.4, 5.1 in subjects with dyslipidemia and 56.9%, 40.4%, 2.6% in subjects without dyslipidemia, respectively. Using a dominant genetic model, subjects carrying C allele (CC&CT genotypes) had a 22% lower risk of dyslipidemia (OR: 0.78, CI 95%: 0.62-0.98 P, 0.03). Individuals with CT vs. TT genotypes had a significantly lower risk of a high serum TC and LDL level. Further analysis showed that there was a positive association between FABP1 genotype (CT) and isolated HTG as well as combined dyslipidemia. The change of a polar amino acid (threonine) in position T94A to a hydrophobic amino acid (alanine) can cause transformation protein. CONCLUSIONS: A CC genotype of the rs2241883 polymorphism of the FABP1 gene appears to confer a higher risk of dyslipidemia in our representative cohort of Iranian individuals.
INTRODUCTION: Dyslipidemia is a known risk factor for cardiovascular disease and is partially determined by genetic variations in the genes involved in lipoprotein metabolism. Therefore, we aimed to assess the association between a polymorphism of the Fatty Acid Binding Protein1 (rs2241883) gene locus and dyslipidemia in an Iranian cohort. MATERIALS AND METHODS: This is a case-control study 2737 individuals were recruited (2203 subjects with dyslipidemia and 534 controls). Dyslipidemia was defined as total cholesterol≥200 mg/dl, or TG≥150 mg/dl, or LDL-C≥130 mg/dl, or HDL-C<40 mg/dl in males and <50 mg/dl in females. Serum lipid profile was determined using a Alcyon Abbott biochemical auto analyzer, USA. Genotyping was made through double amplification refractory mutation system polymerase chain reaction (ARMs PCR). RESULT: The frequency of TT, CT, CC genotypes of rs2241883 polymorphism of FABP1 gene were 65.5, 33.4, 5.1 in subjects with dyslipidemia and 56.9%, 40.4%, 2.6% in subjects without dyslipidemia, respectively. Using a dominant genetic model, subjects carrying C allele (CC&CT genotypes) had a 22% lower risk of dyslipidemia (OR: 0.78, CI 95%: 0.62-0.98 P, 0.03). Individuals with CT vs. TT genotypes had a significantly lower risk of a high serum TC and LDL level. Further analysis showed that there was a positive association between FABP1 genotype (CT) and isolated HTG as well as combined dyslipidemia. The change of a polar amino acid (threonine) in position T94A to a hydrophobic amino acid (alanine) can cause transformation protein. CONCLUSIONS: A CC genotype of the rs2241883 polymorphism of the FABP1 gene appears to confer a higher risk of dyslipidemia in our representative cohort of Iranian individuals.