Association Between Pro12ala Polymorphism of Pparγ2 Gene and Coronary Artery Disease in Iranian Population With Type Two Diabetes Mellitus Publisher



Saremi L¹ ; Lotfipanah S² ; Feizy F³ ; Ghaffari ME⁴ ; Babaniamansour S⁵ ; Saltanatpour Z⁶ Show Affiliations
Source: Acta Endocrinologica Published:2022

Abstract

Context. Coronary artery disease (CAD) is one of the common diseases in patients with type two diabetes mellitus (T2DM). The nuclear hormone receptor peroxisome proliferator-activated receptor-gamma (PPARγ) plays a vital role in dyslipidemia, and oxidative stress is involved in atherogenesis. Objective. The study aimed to determine the association between Pro12Ala polymorphism of the PPARγ2 gene(rs1801282) and CAD risk in T2DM patients in the Iranian population. Design. A group of 145 T2DM patients with a history of CAD were enrolled, together with 145 sex and gender-matched individuals who had neither CAD nor history of T2DM who were enrolled in a case-control study. Subjects and Methods. Polymerase chain reaction-restriction fragment length polymorphism technique was applied to genotype the PPARγ2 gene polymorphisms. Statistical analysis was done using SPSS version 22. Results. CC and GC genotypes of Pro12Ala had a higher frequency in the control and case groups, respectively. The GC genotype was associated with a significantly increased CAD risk compared to the CC genotype (adjusted OR= 2.66, 95% CI = 1.5-29.5, p<0.01). The mean triglycerides and total cholesterol level were significantly higher in the CC genotype than the GC genotype in both case and control groups (p<0.05). The mean level of fasting blood glucose was significantly higher in the CC genotype compared to GC genotype in the case group (p<0.05). The mean of creatinine, lipid profiles, microalbuminuria, and hemoglobin A1c had no significant difference between CC and GC genotypes in both groups (p>0.05). Conclusion. PPARγ2 Pro12Ala polymorphism could be an essential indicator for the increased risk of CAD in the Iranian people with T2DM. © 2022, Acta Endocrinologica Foundation. All rights reserved.