Association of Type II 5 Monodeiodinase Gene Thr92Ala Single Nucleotide Gene Polymorphism in Proved Cardiovascular Disease with Diabetes Mellitus

Abstract

A total of 80 non-smoker, non-alcoholic and clinically proved CVD patients with diabetes were included as case group. Controls: A total 156 non-smoker, non-alcoholic and type 2 diabetes mellitus patients without any sign and symptoms of CVD risk were included as a control group. All the subjects were genotyped for DIO2 T92A and sub-grouped accordingly. Demographic Variables such as age, sex, height, weight, BMI. Genotype Analysis: Type II Deiodinase T92A SNP was determined by using Tetra Primer-ARMS-PCR method. Biochemical Parameters: FPG, HbA1c, fasting Lipid profile, Thyroid function tests, Apo A1, HDL2 and HDL3, D2, paraoxonase, superoxide dismutase; malondialdehyde were analyzed according to standard procedures. Statistical Analysis: Mean±SD was used to explain characteristic of various study parameters. One-way ANOVA was used to find the significant difference between means. The chi-square test was used to find the allelic frequency. Correlation and regression analysis were applied wherever applicable. All statistical tests were done by using PASW 18.0 and Statistica 7 statistical packages. A two tail t-test P lt 0.05 is considered as statistically significant. Results, Discussion and Conclusion: D2 enzyme and THs levels are significantly altered among A/A genotypes when compared to T/T and T/A genotypes. Altered THs have a significant role in the development of secondary dyslipidemia, hyperglycaemia induced oxidative stress and decreased anti-atherogenic function of HDL. In conclusion, this is the first genetic associated study intended to understand the effect of DIO2 T92A polymorphism on thyroid function and the development of cardiovascular disease risk among south Indian type 2 diabetics. Our results show that the DIO2 A/A genotype is associated with altered levels of D2, THs, and HDL3:HDL2 ratio and paraoxonase activity when compared with T/T+T/A genotypes. Our results further indicate that there is a development of thyroid dysfunction among A/A genotypes which resembles like an intrinsic thyroid disease .