Abstract

Increasing evidence showed that telomere length was shorter in age-related diseases, but the mechanism of this phenomenon is still unclear. To determine whether telomere shortening occurs in Type 1 diabetes (T1D) and Type 2 diabetes (T2D), and explore the effect of antioxidant status on the telomere length. T2D patients (no.=62), T1D patients (no.=34), and non-diabetic subjects used as control (CTL) (no.=40) were included in this study. Leukocyte telomere length ratio (T/S ratio) was measured using a quantitative PCR and analyzed. Antioxidant status was estimated by human 8-hydroxy-desoxyguanosine quantization. Other biomarkers, such as fasting plasma glucose, fasting insulin, glycated hemoglobin (HbA1c) and lipid profile were also measured. Compared with CTL group [T/S ratio (mean ± SD), 2.39 ± 0.55], leukocyte telomere length was significantly shorter in T2D group (1.67 ± 0.50) and T1D group (1.77 ± 0.50). 8-OHdG that indicated oxidative stress was significantly higher in T2D (2.99 ± 0.85 ng/ml) and T1D (2.03 ± 0.92 ng/ml) group than in CTL group (0.90 ± 0.46 ng/ml). T/S ratio was significantly negatively correlated with age, waist circumference, waist-to-hip ratio, diastolic blood pressure, fasting plasma glucose, HbA1c, homeostasis model assessment of insulin resistance and 8- OHdG in the whole population. 8-OHdG was independent risk factor for telomere shortening in both T1D (p=0.018) and T2D group (p=0.022). In our study, shorter telomere length and increased oxidative stress were observed in both T1D and T2D. Older people with central obesity, hyperglycemia, insulin resistance and severe antioxidant status tended to have shorter telomere length. In addition, 8- OHdG was an independent predictor for telomere length for both T1D and T2D patients.

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