Abstract 12022: Telomere Length, Telomerase Activity and Vascular Aging in Patients With Type 2 Diabetes Mellitus

Abstract

Introduction: Type 2 diabetes mellitus (T2DM) contribute to vascular aging. The telomere length (TL) and telomerase activity (TA) are considered as biomarkers of cellular aging. TL and TA are insufficiently studied in diabetic patients. Hypothesis: Telomere biology is associated with vascular aging in diabetic patients. Methods: The study group included 50 patients with T2DM (mean age 58.4±7.83 years) and 139 healthy patients (mean age 57.45±8.14 years). All subjects were measured for TL and TA by quantitative polymerase chain reaction; oxidative stress marked by malondialdehyde (MDA); inflammation marked by C-reactive protein (CRP); arterial stiffness evaluated by pulse wave velocity (PWV); carotid intima-media thickness (IMT), plaque presence (PP) and endothelial dysfunction evaluated by flow-mediated endothelium-dependent vasodilation (FMV). Results: All patients were divided into 4 groups by the median of TL (9.75): «short» telomeres (T2DM+ (n=15) and T2DM- (n=63) and «long» telomeres (T2DM+ (n=35) and T2DM- (n=76)). Patients with T2DM and «long» TL had the state of vessels, oxidative stress, inflammation, TA as similar as in healthy people: PWV 11.54±3.57 (T2DM+) vs 10.98±1.83 m/s (T2DM-) ((=0.58), IMT 0.83±0.13 vs 0.76±0.16 mm (=0.13), PP 1.36±0.33 vs 1.23±0.20 (=0.79); MDA 2.81±0.78 vs 3.24±0.78 mkmol/l (=0.08); CRP 3.59±0.58 vs 3.66±0.50 mg/l (=0.93); TA 0.51±0.09 vs 0.60±0.05 (p=0.36). FMV was higher in diabetic patients: 11.87±3.36 vs 10.18±2.79 % (=0.049). In contrast patients with «short» TL and T2DM had more pronounced vascular aging, inflammation and lower TA than healthy people: PWV 13.48±3.24 vs 11.59±2.03 m/s (=0.003), IMT 0.95±0.17 vs 0.78±0.14 mm (<0.001), PP 2.23±0.27 vs 1.38±0.17 (=0.006), FMV 8.51±3.20 vs 11.04±3.01% (=0.0002; CRP 7.39±1.47 vs 4.03±0.62 mg/l (=0.046); TA 0.47±0.08 vs 0.62±0.07 (p=0.06). Conclusion: In patients with short telomeres and T2DM signs of vascular aging, chronic inflammation and cellular aging were more pronounced than in healthy people. In contrast, in patients with long telomeres and T2DM vascular changes, oxidative stress, chronic inflammation and TA were as similar as in healthy people. Perhaps long telomeres protect patients with T2DM from accelerated vascular aging.