Abstract
DNA telomere shortening associates with the age-related increase cardiovascular disease (CVD) risk. Reducing oxidative stress, could modify telomere erosion during cell replication, and CVD risk in patients with chronic kidney disease (CKD). The effect of n-3 fatty acids and coenzyme Q10 (CoQ) on telomere length was studied in a double-blind placebo-controlled trial in CKD. Eighty-five CKD patients were randomized to: n-3 fatty acids (4 g); CoQ (200 mg); both supplements; or control (4 g olive oil), daily for 8 weeks. Telomere length was measured in neutrophils and peripheral blood mononuclear cells (PBMC) at baseline and 8 weeks, with and without correction for cell counts. Main and interactive effects of n-3 fatty acids and CoQ on telomere length were assessed adjusting for baseline values. F2-isoprostanes were measured as markers of oxidative stress. There was no effect of n-3 fatty acids or CoQ on neutrophil or PBMC telomere length. However, telomere length corrected for neutrophil count was increased after n-3 fatty acids (p = 0.015). Post-intervention plasma F2-isoprostanes were negative predictors of post-intervention telomere length corrected for neutrophil count (p = 0.025).The effect of n-3 fatty acids to increased telomere length corrected for neutrophil count may relate to reduced oxidative stress and increased clearance of neutrophils with shorter telomeres from the circulation. This may be a novel mechanism of modifying CVD risk in CKD patients.
Highlights
Telomeres are chromatin structures that cap the ends of chromosomes and preserve genome stability
In a randomized controlled trial that examined the main and additive effects of n-3 fatty acids and coenzyme Q10 (CoQ) on cardiovascular risk in patients with chronic kidney disease (CKD) we showed that n-3 fatty acid supplementation reduced blood pressure, heart rate and plasma triglycerides [22]
Our results show that telomere length corrected for neutrophil count was increased after n-3 fatty acids
Summary
Telomeres are chromatin structures that cap the ends of chromosomes and preserve genome stability. Loss of telomeric DNA eventually leads to cell death or senescence. Telomere shortening has been associated with the age-related increase in risk of chronic conditions such as cancer and cardiovascular disease (CVD). Patients with chronic kidney disease (CKD) and those receiving dialysis. Nutrients 2016, 8, 175 have a greatly increased risk of CVD. There is data from a longitudinal study of patients with stable coronary heart disease suggesting shorter baseline telomere length is associated with lower glomerular filtration rate (GFR) [3]. Patients receiving haemodialysis have shorter telomeres and accelerated telomere shortening compared with the general population [4,5]. Telomere attrition associates with inflammation, low fetuin–A levels and increased mortality in CKD patients undergoing haemodialysis [6]
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