title: Influence of endothelial dysfunction on telomere length in subjects with metabolic syndrome: LIPGENE study.
abstract: 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.
authors.affiliation: Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital/University of Cordoba, Avda. Menendez Pidal, s/n., 14004, Córdoba, Spain.
authors.forename: Lorena
authors.initials: L
authors.lastname: González-Guardia
authors.forename: Elena María
authors.initials: EM
authors.lastname: Yubero-Serrano
authors.forename: Oriol
authors.initials: O
authors.lastname: Rangel-Zuñiga
authors.forename: Carmen
authors.initials: C
authors.lastname: Marin
authors.forename: Antonio
authors.initials: A
authors.lastname: Camargo
authors.forename: Pablo
authors.initials: P
authors.lastname: Pérez-Martínez
authors.forename: Javier
authors.initials: J
authors.lastname: Delgado-Lista
authors.forename: Francisco
authors.initials: F
authors.lastname: Gómez-Delgado
authors.forename: Antonio
authors.initials: A
authors.lastname: Garcia-Rios
authors.forename: Francisco José
authors.initials: FJ
authors.lastname: Tinahones
authors.forename: Helen M
authors.initials: HM
authors.lastname: Roche
authors.forename: Francisco
authors.initials: F
authors.lastname: Pérez-Jiménez
authors.forename: José
authors.initials: J
authors.lastname: López-Miranda
mesh_terms: D000375:Aging / Q000502:physiology*; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology*; D003430:Cross-Sectional Studies; D004247:DNA / Q000235:genetics*; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D005060:Europe / Q000453:epidemiology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D015994:Incidence; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000235:genetics / Q000378:metabolism*; D008875:Middle Aged; D018384:Oxidative Stress; D016133:Polymerase Chain Reaction; D016615:Telomere / Q000235:genetics* / Q000378:metabolism; D014664:Vasodilation / Q000502:physiology*
chemical_list: D004247:DNA