Influence of endothelial dysfunction on telomere length in subjects with metabolic syndrome: LIPGENE study

Previous evidences support that increased oxidative stress (OxS) may play an important role in metabolic syndrome (MetS) and both are closely linked to vascular dysfunction. This study determined whether there is a relationship between endothelial function and relative telomere length (RTL) in MetS...

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Veröffentlicht in:AGE 2014, Vol.36 (4), p.9681-9681, Article 9681
Hauptverfasser: González-Guardia, Lorena, Yubero-Serrano, Elena María, Rangel-Zuñiga, Oriol, Marin, Carmen, Camargo, Antonio, Pérez-Martínez, Pablo, Delgado-Lista, Javier, Gómez-Delgado, Francisco, Garcia-Rios, Antonio, Tinahones, Francisco José, Roche, Helen M., Pérez-Jiménez, Francisco, López-Miranda, José
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Sprache:eng
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Zusammenfassung:Previous evidences support that increased oxidative stress (OxS) may play an important role in metabolic syndrome (MetS) and both are closely linked to vascular dysfunction. This study determined whether there is a relationship between endothelial function and relative telomere length (RTL) in MetS subjects. In this cross-sectional study from the LIPGENE cohort, a total of 88 subjects (36 men and 52 women) were divided into four groups by quartiles of telomere length. We measured ischemic reactive hyperemia (IRH), total nitrite (NO) and protein carbonyl (PC) plasma levels, F2-isoprostanes urinary levels, and superoxide dismutase (SOD) and glutathione peroxidase (GPx) plasma activities. IRH and NO plasma levels were higher in subjects with longer RTL (quartiles 3 and 4), while PC plasma levels, F2-isoprostanes urinary levels, and GPx and SOD plasma activities were lower in quartile 4 subjects (longest RTL). Additionally, MetS subjects with longer RTL had greater homeostatic model assessment-β level and lower triglycerides plasma levels. Our results suggest that endothelial dysfunction, associated with high levels of OxS, could be entailed in an increment of telomere attrition. Thus, further support of the molecular and cellular mechanisms involved in vascular dysfunction may contribute to the development of strategies to decelerate vascular aging or prevent cardiovascular disease.
ISSN:0161-9152
2509-2715
1574-4647
2509-2723
DOI:10.1007/s11357-014-9681-9