Background: Genomic damage plays an important role in the pathogenesis of Type 2 Diabetes Mellitus (T2DM) and its complications. This instability increases with impaired metabolic control, and is aggravated by the presence of advance glycation-end products (AGEs) causing more cell damage. The aim of this study was to analyse the presence of genomic instability in patients with T2DM and its association with the levels of AGEs, namely glycated haemoglobin (HbA1c) and glycated albumin (GA)
Patients and methods: The study design was observational, cross-sectional, and comparative with 36 participants diagnosed with T2DM, attending an Endocrinology Service in a Regional Hospital in Yucatán, México. The main inclusion criteria were: an evolution time of the disease of at least 3 years and having been a resident of the region of at least 10 years. We included 12 healthy subjects as a control group. All volunteers were tested for plasma glucose, HbA1c, GA, and body composition. The genomic instability determination was performed by single cell gel electrophoresis (comet assay), using peripheral blood mononuclear cells, fluorescence microscopy and a special software for image analysis.
Results: Between 75 and 81% of the T2DM participants showed some degree of impaired metabolic control with higher levels of HbA1c, GA or both. The genomic instability showed a significant association for high degree of DNA fragmentation and T2DM participants (P=0.032). Correlation analysis demonstrated that higher serum GA levels had higher comet length tail (indicating higher instability) when cells were exposed to oxidative stress (P=0.024). Among other findings, waist girth was significantly correlated with higher DNA fragmentation (P=0.044).
Conclusion: Although there is evidence that T2DM is associated to genomic instability, we showed that higher levels of GA are associated to a higher genomic instability, and according to some authors, this biomarker could represent a better indicator than HbA1c for metabolic impairment.