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Abstract Background Type 2 diabetes (T2D) is a complex trait in humans. Several environmental and hereditary factors contribute to the overall pathogenesis of this disease. The association between genes, environment, and T2D was unknown for decades until epigenetics was discovered. Epigenetics affects gene transcription, which, in turn, influences organ function. One of the epigenetic regulatory mechanisms is DNA methylation. This mechanism permits modification of gene function without changes in the DNA sequence. There are several risk factors for type 2 diabetes such as harmful intrauterine environment, obesity, poor physical activity, increasing age, a family history of the disease, and an unhealthy diet. All these factors have been proven to influence the DNA methylation sequence in target tissues for insulin resistance in humans. We aimed to evaluate insulin-like growth factor binding protein-1 (IGFBP1) gene methylation levels in T2D. In all, 100 Egyptian individuals were included in this study: 50 patients with T2D versus 50 healthy controls. Genomic DNA was extracted from peripheral blood and IGFBP1 methylation levels were analyzed using pyrosequencing. Results DNA methylation levels in the IGFBP1 gene at each of the six CpG sites were significantly higher in the T2D patients than in the controls at P values of 0.001, 0.002, 0.010, 0.007, 0.014, and 0.001, respectively. Conclusion According to this study, T2D is due to interactions between genetics, epigenetics, and lifestyle. This study also revealed that DNA methylation levels of the IGFBP-1 gene are higher in T2D patients than in healthy control. |
