Zahra Kalantar1, Mohamad Reza Eshraghian2, Gity Sotoudeh3, Mahmoud Djalali1, Anahita Mansouri4, Ehsan Alvandi1, Fatemeh Javadi5, Maryam Mahmoudi1, Fariba Koohdani6. 1. Department of Cellular and Molecular Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran. 2. Department of Biostatistics and Epidemiology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. 3. Department of Community Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran. 4. Nutrition and Metabolic Diseases Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. 5. School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran. 6. Department of Cellular and Molecular Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran; Diabetic Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: fkoohdan@tums.ac.ir.
Abstract
BACKGROUND & AIM: Dyslipidemia is one of the major complications in patients with type 2 diabetes mellitus (T2DM). Dietary fat intake and genetic factors including CETP Taq1B polymorphism could also affect lipid profile concentrations, in particular HDL-c. We decided to study the frequency of this polymorphism and its interaction with dietary fat intake on HDL-c concentration among Iranian T2DM patients with and without dyslipidemia. METHODS: In this comparative study, serum samples were collected from 55 patients with dyslipidemia and 129 patients without dyslipidemia. Validated semi-quantitative FFQ was used for food consumption data. CETP Taq1B polymorphism was studied by polymerase chain reaction-restriction length polymorphism (PCR-RFLP). We used χ2 and two-way ANOVA tests for statistical analysis. RESULTS: The frequency of B1B1 genotype was higher in patients with dyslipidemia (p = 0.01). There was no significant relationship between CETP Taq1B polymorphism and lipid profile concentrations. In patients without dyslipidemia, the interaction between the polymorphism and total fat intake on HDL-c concentration as well as TG/HDL ratio was significant (p = 0.02 and p = 0.009 respectively). This was more evident in B1B1 genotype. Moreover, HDL-c concentration was significantly higher in B2B2 genotype with low total fat intake. CONCLUSION: Higher total fat intake may affect the relationship between CETP Taq1B polymorphism and HDL-c concentration in patients with normolipidemic T2DM.
BACKGROUND & AIM: Dyslipidemia is one of the major complications in patients with type 2 diabetes mellitus (T2DM). Dietary fat intake and genetic factors including CETP Taq1B polymorphism could also affect lipid profile concentrations, in particular HDL-c. We decided to study the frequency of this polymorphism and its interaction with dietary fat intake on HDL-c concentration among Iranian T2DM patients with and without dyslipidemia. METHODS: In this comparative study, serum samples were collected from 55 patients with dyslipidemia and 129 patients without dyslipidemia. Validated semi-quantitative FFQ was used for food consumption data. CETP Taq1B polymorphism was studied by polymerase chain reaction-restriction length polymorphism (PCR-RFLP). We used χ2 and two-way ANOVA tests for statistical analysis. RESULTS: The frequency of B1B1 genotype was higher in patients with dyslipidemia (p = 0.01). There was no significant relationship between CETP Taq1B polymorphism and lipid profile concentrations. In patients without dyslipidemia, the interaction between the polymorphism and total fat intake on HDL-c concentration as well as TG/HDL ratio was significant (p = 0.02 and p = 0.009 respectively). This was more evident in B1B1 genotype. Moreover, HDL-c concentration was significantly higher in B2B2 genotype with low total fat intake. CONCLUSION: Higher total fat intake may affect the relationship between CETP Taq1B polymorphism and HDL-c concentration in patients with normolipidemic T2DM.