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. (C)
2011 Elsevier B.V. All rights reserved