Role of Mitochondrial DNA in Development of Type 2 Diabetes Mellitus with/without Ischemic Heart Diseases of Iraqi Patients

Abstract

Objectives: This study aimed to investigate the associations between various biomarkers and the specific mutation of mitochondrial DNA in type 2 diabetes mellitus with ischemic heart diseases and compared with T2DM patients without ischemic heart disease.

Methods: The study select two groups of patients admitted to Kerbala Heart Center and Al-Hassan Center for Endocrinology and Diabetes, Al-Hussein Teaching Hospital, Al-Hussein Medical City, Kerbala Health Directorates / Kerbala – Iraq between Nov., 2020 and Aug., 2021. The first group includes 50 patients of type 2 diabetes mellitus with ischemic heart disease (28 male and 22 female) with age ranged between 45-76 years, and the second group includes another 50 patients with type 2 diabetes mellitus without ischemic heart disease (24 male and 26 female) with age ranged between 49-82 years. Fasting serum glucose, insulin and insulin resistance have been determined and then correlated with nutation mitDNA investigated in sera of T2DM with/without ischemic heart diseases.

Results: The amplification of the MTLL1 gene gives one genotypes as indicated by (422 bp) bands for those with homozygous wild type (AA), homozygous mutant (GG) genotypes and two genotypes bands (422 bp) for those with heterozygous (GA). The obtained data revealed that a strong positive correlation between Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) and insulin (r = 0.926) with significant differences (P<0.05) was obtained in the sera of type 2 diabetic patient with ischemic heart disease as compared with that obtained in type 2 diabetic patients without ischemic heart diseases.

Conclusion: The prevalence of association between HOMA-IR with MTTL1 G3243A mutation (GG allele) in type 2 diabetic patients with ischemic heart disease was only 8.0% and may be associated with maternally inherited of type 2 diabetes mellitus with ischemic heart disease as a pathogenic mutation in Iraqi population.