Assessing the relationship between Iraqi patients' risk of type 2 diabetes and genetic variations in the CYP17A1 gene

Abstract

The characteristic feature of type 2 diabetes mellitus is a rise in blood sugar (glucose) because of insufficient insulin secretion from pancreatic beta cells, ineffective insulin, somatic cell resistance to insulin, or a combination of these factors. The purpose of this study is to assess the impact of CYP17A1 genetic polymorphisms at the rs6163 and rs6162 variant sites on the risk of type II diabetes. The tenth chromosome's mitochondrial CYP17A1 gene is linked to high blood pressure, insulin resistance, and polycystic ovarian syndrome in addition to encoding a crucial enzyme involved in the manufacture and metabolism of steroid hormones. As the homologous genetic genotype AA and allele A showed an increase in the diabetic group, the study's results demonstrated the presence of genetic heterogeneity at the site of heterogeneity C/A rs6163 in the gene CYP17A1. This is a causative factor according to the Fisher's probability, as the probability value (P = 0.026) as there are significant differences between patients and healthy people, and according to the values of the odd ratio, which reached 9.47 and 2.80, respectively. According to the Fisher's probability, the homogeneous genetic type CC and allele C are protective factors against the disease. The probability value was (P = 0.055), indicating that there are significant differences between patients and healthy individuals. The odds ratio values reached 0.24 and 0.36. According to the probability of Frisher, the homogeneous genotype GG and allele G are protective factors; the probability value is (P = 0.226), where there are no significant differences between patients and healthy individuals, and according to the value of the odds ratio, which amounted to (0.44 and 0.42), respectively. The study's results indicated the presence of genetic heterogeneity at the site of the heterogeneity, rs6162 G/A. According to the Fisher's probability, genotype AA and allele A are regarded as causal agents; the corresponding odds ratio values were 2.80 and 9.47, respectively. The p-value was found to be (P = 0.026).