Chromosomal Aberrations (mean ± SD†)
Groups	Deletion	Translocation	Inversion	Total	MN‡ /1000 cells (mean ± SD)
Experimental	1.41±1.30	0.91±0.79	0.44±0.56	2.76±1.65*	13.28±8.63*
Control	0.15±0.36	0.18±0.46	0.15±0.43	0.47±0.75	4.12±8.89

†SD- standard deviation; ‡MN- micronucleus * values are significant at p<0.05 when compared to control samples.

The patients showed different types of CA such as deletion, translocation and inversion. About 95% of the diabetic patients were found to have more than one aberration. The subjects of age 49 and above had more number of chromosomal anomalies (≥4) when compared to people of other age groups. From the data it was observed that deletion is the major aberration among the experimental subjects.

In the control population, 12 subjects showed one or the other anomalies. Translocation was the frequently observed type of aberration among the control samples. When compared to control population,experimental subjects showed higher rates of chromosomal damage. The total frequency ofchromosomal anomalies of experimental group was found to be 2.76 ± 1.65 which is significantly higher than the control group whose frequency was 0.47 ± 0.75. This was proved statistically using Z-test. The frequencies of deletion, translocation and inversion in the experimental group were found to be 1.41 ± 1.30, 0.91 ± 0.79 and 0.44 ± 0.56 respectively. Meanwhile, the control group showed the frequencies to be 0.15 ± 0.36, 0.18 ± 0.46 and 0.15 ± 0.43 respectively. The percentage of micronuclei in experimental participants was observed to be 13.28±8.63 and that of control group was 4.12 ± 8.89. The MN percentage of the diabetic group was also significantly higher than the control group which was statistically established using Z – test. When analyzed through Pearson’s correlation test total CA and duration of diabetes showed moderate positive correlation though there was no significant relationship between total CA and BMI.

Type 2 diabetes which is a hyperglycemic condition is associated with genetic and chromosomal variations. The abnormalities can be attributed to increased release of highly reactive oxygen free radicals [12]. Increased release of interleukins can lead to ROS production which indeed cause insulin resistance and β- cell dysfunction which are characteristics of T2DM. The hyperglycemic state results in glycation of proteins and auto-oxidation of glucose which augments the formation of ROS [14]. Genotoxicity studies such as chromosomal aberration (CA) assay and micronucleus (MN) assay are common methods to analyze the anomalies. There are several studies establishing chromosomal damages in T2DM patients. From the present study it was found that diabetic patients have significant chromosomal aberrations when compared to the control group. Boehm et al (2008) showed that T2DM women carry stable chromosomal aberrations when compared to healthy subjects [9]. They suggested that these stable oddities can be a senescence marker of premature death in diabetic women. Body Mass Index (BMI) has strong association with diabetes. Obesity leading to insulin resistance and impaired insulin secretion can often be a major cause of T2DM [5]. Overweight individuals are at higher risk to have DNA damage due to oxidative stress [1]. In the study it was observed that the experimental group had higher BMI values than control subjects. But there was no significant correlation between total CA and BMI in the experimental group. The formation of micronucleus is another parameter which determines the extent of DNA abnormalities. According to Corbi et al., (2014) reported elevated micronucleus formation in diabetic patients [1]. These people had high number of binucleated cells with micronuclei and nucleoplasmic bridges. Shettigar et.al., (2012) observed modest increase in MN frequency in poorly controlled diabetic patients [12]. According to the study conducted by Bronson et.al.,(2015) frequency of MN increases with duration of diabetes in the experimental samples [11]. The results of thecurrent study are also in accordance with the previous studies and shows increased MN frequency in diabetic group. Nevertheless, few studies showed no linkage between diabetes and increased DNA damageand this can be due to duration of the disease in the patients considered for the particular study [15]. As per the study by [16] it the percentage of sister chromatid exchange (SCE), duration of diabetes and age in type-1 mellitus patients showed no significant correlation though the present study reported a moderate positive correlation between total CA and duration of diabetes.

Genotoxic studies are very much important in diseases like T2DM which causes psychological and physical stress to patients and put a huge burden on health-care systems. The extent of DNA damage increases the chances of microvascular and macrovascular complications such as dyslipidemia, periodontitis, cardiovascular diseases and neuropathy which are often associated with diabetes. The chromosomal anomalies are the result of oxidative damage caused by ROS.Oxidative stress over time can cause structural and functional changes in chromosomes. This can often cause diseased conditions like cancer [16]. As the primary objective of any treatment strategy is to slow down the progression of metabolic deterioration, it is important to establish methods for early disease identification and disease management. This can be done by conducting further cytogenetic studies with a large sample size in order to analyze the genetic conditions in diabetic patients.