title: "Is obesity linked to aging?": adipose tissue and the role of telomeres.
abstract: Obesity is a condition in which excess or abnormal fat accumulation may present with adverse effects on health and decreased life expectancy. Increased body weight and adipose tissue accumulation amplifies the risk of developing various age-related diseases, such as cardiovascular disease, type 2 diabetes mellitus, musculoskeletal disorders, respiratory diseases and certain types of cancer. This imbalance in body composition and body weight is now recognized as a state of increased oxidative stress and inflammation for the organism. Increasing oxidative stress and inflammation affect telomeres. Telomeres are specialized DNA-protein structures found at the ends of eukaryotic chromosomes and serve as markers of biological aging rate. They also play a critical role in maintaining genomic integrity and are involved in age-related metabolic dysfunction. Erosion of telomeres is hazardous to healthy cells, as it is a known mechanism of premature cellular senescence and loss of longevity. The association of telomeres and oxidative stress is evident in cultured somatic cells in vitro, where oxidative stress enhances the process of erosion with each cycle of replication. Shorter telomeres have been associated with increasing body mass index, increased adiposity, and more recently with increasing waist to hip ratio and visceral excess fat accumulation. Furthermore, many of the metabolic imbalances of obesity (e.g. glycemic, lipidemic, etc.) give rise to organ dysfunction in a way that resembles the accelerated aging process. This article is a non-systematic review of the evidence linking obesity and accelerated aging processes as they are regulated by telomeres.
authors.affiliation: Laboratory for Experimental Surgery and Surgical Research "N. S. Christeas", University of Athens Medical School, Greece. itzanetakoy@yahoo.gr
authors.forename: Irene P
authors.initials: IP
authors.lastname: Tzanetakou
authors.forename: Nikolaos L
authors.initials: NL
authors.lastname: Katsilambros
authors.forename: Athanase
authors.initials: A
authors.lastname: Benetos
authors.forename: Dimitrios P
authors.initials: DP
authors.lastname: Mikhailidis
authors.forename: Despina N
authors.initials: DN
authors.lastname: Perrea
mesh_terms: D000273:Adipose Tissue / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000235:genetics* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D000818:Animals; D016922:Cellular Senescence; D002648:Child; D002675:Child, Preschool; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000235:genetics* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D016615:Telomere / Q000378:metabolism*; D059506:Telomere Shortening; D055815:Young Adult
chemical_list: D018836:Inflammation Mediators