Type 2 Diabetes From the Perspective of Telomere Biology

BACKGROUND: Type 2 diabetes mellitus (T2DM) has emerged as one of the most critical public health challenges worldwide, with its prevalence continuing to rise steadily. Current projections estimate that the global number of individuals affected by T2DM will reach approximately 783 million by 2045, imposing an increasingly severe burden on healthcare systems globally. In recent years, growing attention has been directed toward the relationship between telomere biology and metabolic disorders. Telomeres, the protective structures at the ends of chromosomes, serve as key markers of cellular aging, with their length and integrity reflecting biological age. Telomerase, a specialised enzyme complex, plays a central role in maintaining telomere stability. Accumulating evidence suggests that telomere shortening and dysfunction not only accelerate organismal aging but may also contribute to the pathogenesis of T2DM through multiple molecular pathways. OBJECTIVE: This review aims to systematically synthesise recent research advances regarding the association between telomeres and T2DM, and to explore the clinical translational potential of telomere length and telomerase activity as biomarkers of disease risk or as potential therapeutic targets. METHODS: A systematic search of relevant articles was conducted across databases including PubMed, Web of Science, and CNKI. Search terms comprised 'Telomere', 'Telomerase', 'T2DM' and 'Treatment'. Through screening and integration of evidence from cellular experiments, animal model studies, population-based epidemiological investigations and clinical observational research, this review systematically synthesises the mechanistic evidence and current research landscape regarding the association between telomeres and T2DM. RESULTS: Accumulating evidence consistently indicates a significant association between telomere biology and the development and progression of T2DM. Key mechanisms primarily involve oxidative stress and cellular apoptosis, while telomere dysfunction may also contribute to glucose metabolism disorders by impairing pancreatic β-cell function and peripheral tissue insulin sensitivity. Dynamic changes in telomeres hold promise as novel biomarkers for assessing T2DM risk and disease progression. CONCLUSIONS: A close and bidirectional relationship exists between telomere biology and T2DM. Deeper insights into this association not only enhance our understanding of T2DM pathogenesis but also offer potential therapeutic targets for anti-aging-based interventions, highlighting important clinical translation prospects. Future research should further clarify the causal relationships involved and explore strategies aimed at preserving telomeres or modulating telomerase activity to delay diabetes progression and prevent its complications, thereby advancing novel approaches for early risk assessment and precision management of T2DM.