What is it about?
We examined the associations of two biomarkers of oxidative stress with new type 2 diabetes diagnoses in 7,828 individuals initially without diabetes from a population-based German cohort study with 14 years of follow-up. No associations were found in the youngest age-group (50–59 years) but strong and robust associations were detected for both biomarkers in the oldest age-group (65–75 years) of the cohort. 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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Why is it important?
We think that this original research is of utmost interest to readers because only three, small prospective studies (n < 222 type 2 diabetes cases) have been published on this research topic before and they had conflicting results. As cellular oxidative stress is volatile and can be improved by a healthy life-style (smoking cessation, healthy diet, physical activity) it can be a target for type 2 diabetes prevention.
Perspectives
The overarching mechanism might be an accumulation of oxidative damage of cell compartments over time that overwhelms the cellular repair mechanisms in aged cells. Regarding pancreatic β-cells, pancreatic islets are very prone to damage by free radicals because they have a high metabolic activity and a particularly low expression of antioxidant enzymes. Thus, oxidative stress in ß-cells can lead to impaired glucose-stimulated insulin secretion or even apoptosis of ß-cells. Furthermore, oxidative stress can cause insulin resistance by disrupting the insulin receptor signalling pathway.
Ben Schöttker
German Cancer Research Center
Read the Original
This page is a summary of: 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, Diabetes Care, October 2019, American Diabetes Association,
DOI: 10.2337/dc19-1379.
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