Abstract
Cellular aging markers, including telomere length and mitochondrial function, as well as oxidative stress and inflammation markers influence each other and form a complex network, which is affected in diabetes. However, it remains unknown whether these markers could independently predict future diabetes after adjustment for their mutual effects. We conducted a 3-year longitudinal study in a Chinese cohort that comprised 108 nondiabetic individuals at baseline. The 2-hour 75 g oral glucose tolerance tests were performed at baseline and at 3-year follow-up. At baseline, leukocyte telomere length (LTL) and mitochondrial DNA copy number (mtDNAcn) in leukocytes were determined using the polymerase chain reaction method. Tumor necrosis factor (TNF-α), interleukin-6, 8-hydroxy-2-deoxyguanosine levels, and superoxide dismutase (SOD) activity were measured by the enzyme-linked immunosorbent assay. Participants who developed diabetes at the 3-year follow-up (n = 28) had shorter LTL and higher levels of TNF-α and SOD activity at baseline. Baseline LTL was found to be independently associated with the development of diabetes at the 3-year follow-up after the adjustment for mtDNAcn, markers of oxidative stress and inflammation, and conventional diabetes risk factors. Our findings suggest that LTL is an independent predictor for 3-year diabetes risk, which might inform timely prevention and treatment of diabetes. Telomere shortening might be involved in the pathogenesis of diabetes independently of conventional diabetes risk factors, mtDNAcn, or oxidative stress and inflammation pathways.
Highlights
Over the last several decades, numerous studies have revealed that telomere length, mitochondrial function, oxidative stress, and inflammation are cellular aging markers intertwined in the complex relationships that determine their roles in cellular senescence [1,2,3]
In a multiracial cohort of postmenopausal women, just a weak association was found between baseline leukocyte telomere length (LTL) and future diabetes risk, which was attenuated after adjusting for conventional diabetes risk factors [15]
We considerably extended the conclusions of those reports by showing that the correlation between LTL for diabetes risk is independent of mitochondrial DNA copy number (mtDNAcn) and markers of oxidative stress and inflammation
Summary
Over the last several decades, numerous studies have revealed that telomere length, mitochondrial function, oxidative stress, and inflammation are cellular aging markers intertwined in the complex relationships that determine their roles in cellular senescence [1,2,3] These cellular aging markers have been reported to be associated with various age-related diseases [4, 5], including diabetes [6, 7]. Considering the complex relationships between these biomarkers, it should be established whether they could affect each other’s predictive role in diabetes risk Taking into account these considerations, we conducted a 3-year longitudinal study in a Chinese population to investigate the prospective associations of baseline LTL and mtDNAcn, as well as oxidative stress and inflammatory markers with the development of diabetes 3 years later
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