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High sodium intake is associated with short leukocyte telomere length in overweight and obese adolescents

BACKGROUND/OBJECTIVES: Telomere shortening plays an important role in cellular aging. However, the impact of high sodium intake, an important risk factor of age-related diseases, on telomere shortening remains unknown. Therefore, we examined the relationship between high dietary sodium intake and le...

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Detalles Bibliográficos
Autores principales: Zhu, Haidong, Bhagatwala, Jigar, Pollock, Norman K., Parikh, Samip, Gutin, Bernard, Stallmann-Jorgensen, Inger, Thomas, Jeffrey, Harshfield, Gregory A., Dong, Yanbin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6344938/
https://www.ncbi.nlm.nih.gov/pubmed/25869605
http://dx.doi.org/10.1038/ijo.2015.51
Descripción
Sumario:BACKGROUND/OBJECTIVES: Telomere shortening plays an important role in cellular aging. However, the impact of high sodium intake, an important risk factor of age-related diseases, on telomere shortening remains unknown. Therefore, we examined the relationship between high dietary sodium intake and leukocyte telomere length, particularly in the context of obesity since obesity increases salt sensitivity. SUBJECTS/METHODS: Leukocyte telomere length (LTL) was determined by a quantitative polymerase chain reaction method in 766 adolescents aged 14–18 years (50% female, 49% African Americans). Dietary sodium intake was assessed by seven independent 24-h dietary recalls. We divided the sample into low sodium (mean 2388 ± 522 mg/day) or high sodium groups (mean 4142 ± 882 mg/day) based on the median value (3280.9 mg/day). RESULTS: In the entire cohort, there was no significant association between sodium intake and LTL (r = −0.05, p = 0.24). However, there was a significant interaction between sodium intake and obesity status (p = 0.049). Further multiple linear regression analyses revealed that higher dietary sodium intake was associated with shorter LTL in the overweight/obese group (BMI ≥ 85(th) percentile, β = −0.37, p = 0.04), but not in the normal weight group (β = 0.01, p= 0.93) after adjusting for multiple confounding factors. In the overweight/obese group, LTL was significantly shorter in the high sodium intake subjects vs. low sodium intake subjects (1.24 ± 0.22 vs. 1.32 ± 0.20, p = 0.02), but not the normal weight group (1.29 ± 0.24 vs. 1.30 ± 0.24, p = 0.69). CONCLUSIONS: Higher dietary sodium intake is associated with shorter telomere length in overweight and obese adolescents.