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| Home > Publications database > Oxidatively Damaged DNA/RNA and 8-Isoprostane Levels Are Associated With the Development of Type 2 Diabetes at Older Age: Results From a Large Cohort Study. |
| Home > Publications database > Oxidatively Damaged DNA/RNA and 8-Isoprostane Levels Are Associated With the Development of Type 2 Diabetes at Older Age: Results From a Large Cohort Study. |
| Journal Article | DKFZ-2019-02504 |
; ; ; ;
2020
Assoc.
Alexandria, Va.
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Please use a persistent id in citations: doi:10.2337/dc19-1379
Abstract: Oxidative stress is believed to play an important role in the pathophysiology of type 2 diabetes, but the few cohort studies that have assessed the association of oxidative stress biomarkers with type 2 diabetes incidence were small and reported inconclusive results.We examined the associations of urinary oxidized guanine/guanosine (OxGua) levels (a biomarker of DNA/RNA oxidation) and urinary 8-isoprostane levels (a biomarker of lipid peroxidation) with type 2 diabetes incidence in 7,828 individuals initially without diabetes from a population-based German cohort study with 14 years of follow-up. Hazard ratios (HRs) and 95% CIs per 1 SD were obtained using multivariable-adjusted Cox proportional hazards regression models.In the total population, weak but statistically significant associations with type 2 diabetes incidence were observed for OxGua (HR [95% CI] per 1 SD 1.05 [1.01; 1.09]) and 8-isoprostane (1.04 [1.00; 1.09]) levels. Stratified analyses showed that associations of both biomarkers with type 2 diabetes incidence were absent in the youngest age-group (50-59 years) and strongest in the oldest age-group (65-75 years) of the cohort, with HRs of OxGua levels of 1.14 (1.05; 1.23) per 1 SD and of 8-isoprostane levels of 1.22 (1.02; 1.45) per 1 SD.These results from a large cohort study support suggestions that an imbalanced redox system contributes to the development of type 2 diabetes but suggest that this association becomes clinically apparent at older ages only, possibly as a result of reduced cellular repair capacity.
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