The Long and Short of Telomere Length and Diabetes

  1. Robert A. Scott
  1. MRC Epidemiology Unit, University of Cambridge, Cambridge, U.K.
  1. Corresponding author: Robert A. Scott, robert.scott{at}mrc-epid.cam.ac.uk.

Aging is a major risk factor for a number of complex diseases including cancers, cardiovascular disease, and type 2 diabetes, yet the biological processes linking aging and disease risk are poorly understood. A potential mediator of age-related increases in disease risk may lie in repetitive sequences of DNA known as telomeres. Telomeres represent the genome’s defense mechanism against the biological conundrum that the tail ends of chromosomes cannot be replicated when cells divide (1). During mitosis, telomeric DNA is sacrificed in return for protecting the protein coding and regulatory elements of the genome, and as a result they become shorter with cellular aging (2). The enzyme telomerase helps to guard against this telomere loss by making additional copies of the hexanucleotide repeats that make up these protective chromosomal caps (3). However, when a critical threshold of shortening is reached (the “Hayflick limit”), cell senescence follows (4).

While telomeres are shorter in older age (5), the rate of telomere shortening varies among individuals (6). The association of shorter telomeres with disease and mortality (7) implicates telomeres as a biomarker of biological aging (8). Telomere shortening is influenced by a range of cellular stressors (9) such that telomere length may lie on the causal pathway between lifestyle exposures and risk of disease. Previous studies have highlighted the role of health behaviors in …

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