Shorter telomeres are associated with obesity and weight gain in the elderly

Department of Medicine, University of California, San Francisco, San Francisco, CA, USA.
International journal of obesity (2005) (Impact Factor: 5). 10/2011; 36(9):1176-9. DOI: 10.1038/ijo.2011.196
Source: PubMed


Objective:Obesity and shorter telomeres are commonly associated with elevated risk for age-related diseases and mortality. Whether telomere length (TL) may be associated with obesity or variations in adiposity is not well established. Therefore, we set out to test the hypothesis that TL may be a risk factor for increased adiposity using data from a large population-based cohort study.Design:Levels of adiposity were assessed in six ways (obesity status, body mass index (BMI), the percentage of body fat or % body fat, leptin, visceral and subcutaneous fat mass) in 2721 elderly subjects (42% black and 58% white). Associations between TL measured in leukocytes at baseline and adiposity traits measured at baseline, and three of these traits after 7 years of follow-up were tested using regression models adjusting for important covariates. Additionally, we look at weight changes and relative changes in BMI and % body fat between baseline and follow-up.Results:At baseline, TL was negatively associated with % body fat (ß=-0.35±0.09, P=0.001) and subcutaneous fat (ß=-2.66±1.07, P=0.01), and positively associated with leptin after adjusting for % body fat (ß=0.32±0.14, P=0.001), but not with obesity, BMI or visceral fat. Prospective analyses showed that longer TL was associated with positive percent change between baseline and 7-year follow-up for both BMI (ß=0.48±0.20, P=0.01) and % body fat (ß=0.42±0.23, P=0.05).Conclusion:Our study suggests that shorter TL may be a risk factor for increased adiposity. Coupling with previous reports on their reversed roles, the relationship between adiposity and TL may be complicated and may warrant more prospective studies.

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    • "Telomeres play an important role in maintaining genomic stability and regulating cellular replicative capacity (Allsopp et al., 1992; Blackburn et al., 2006). Telomere length is heritable, and length declines with increasing age (Njajou et al., 2012; Nordfjall et al., 2005; Shammas, 2011). Especially in early life, the impact of inheritance on telomere length is strong, but it seems to diminish by age (Svenson et al., 2011). "
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    ABSTRACT: A career as an elite-class male athlete seems to improve metabolic heath in later life and is also associated with longer life expectancy. Telomere length is a biomarker of biological cellular ageing and could thus predict morbidity and mortality. The main aim of this study was to assess the association between vigorous elite-class physical activity during young adulthood on later life leukocyte telomere length (LTL). The study participants consist of former male Finnish elite athletes (n = 392) and their age-matched controls (n = 207). Relative telomere length was determined from peripheral blood leukocytes by quantitative real-time polymerase chain reaction. Volume of leisure-time physical activity (LTPA) was self-reported and expressed in metabolic equivalent hours. No significant difference in mean age-adjusted LTL in late life (p = 0.845) was observed when comparing former male elite athletes and their age-matched controls. Current volume of LTPA had no marked influence on mean age-adjusted LTL (p for trend 0.788). LTL was inversely associated with age (p = 0.004).Our study findings suggest that a former elite athlete career is not associated with LTL later in life. Key pointsA career as an elite-class athlete is associated with improved metabolic health in late life and is associated with longer life expectancy.A career as an elite-class athlete during young adulthood was not associated with leukocyte telomere length in later life.Current volume of leisure-time physical activity did not influence telomere length in later life.
    Journal of sports science & medicine 06/2015; 14(2):239-45. · 1.03 Impact Factor
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    • "It has been shown that individuals with obesity, type 2 diabetes (T2D) and additional cardiovascular risk factors have shortened telomeres in the peripheral blood and in SAT [1] [7]. The TL in circulating blood cells is negatively associated with age, BMI, hip and waist circumference, systolic blood pressure, triglycerides, fasting glucose levels and body fat percentage [1]. "
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    ABSTRACT: Adipocyte hypertrophy and hyperplasia have been shown to be associated with shorter telomere length, which may reflect aging, altered cell proliferation and adipose tissue (AT) dysfunction. In individuals with obesity, differences in fat distribution and AT cellular composition may contribute to obesity related metabolic diseases. Here, we tested the hypotheses that telomere lengths (TL) are different between: (1) abdominal subcutaneous and omental fat depots, (2) superficial and deep abdominal subcutaneous AT (SAT), and (3) adipocytes and cells of the stromal vascular fraction (SVF). We further asked whether AT TL is related to age, anthropometric and metabolic traits. TL was analyzed by quantitative PCR in total human genomic DNA isolated from paired subcutaneous and visceral AT of 47 lean and 50 obese individuals. In subgroups, we analyzed TL in isolated small and large adipocytes and SVF cells. We find significantly shorter TL in subcutaneous compared to visceral AT (p<0.001) which is consistent in men and subgroups of lean and obese, and individuals with or without type 2 diabetes (T2D). Shorter TL in SAT is entirely due to shorter TL in the SVF compared to visceral AT (p<0.01). SAT TL is most strongly correlated with age (r=-0.205, p<0.05) and independently of age with HbA1c (r=-0.5, p<0.05). We found significant TL differences between superficial SAT of lean and obese as well as between individuals with our without T2D, but not between the two layers of SAT. Our data indicate that fat depot differences in TL mainly reflect shorter TL of SVF cells. In addition, we found an age and BMI-independent relationship between shorter TL and HbA1c suggesting that chronic hyperglycemia may impair the regenerative capacity of AT more strongly than obesity alone. Copyright © 2015. Published by Elsevier Inc.
    Biochemical and Biophysical Research Communications 01/2015; 457(3). DOI:10.1016/j.bbrc.2014.12.122 · 2.30 Impact Factor
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    • "Telomere length (TL) is likely influenced not only by genetic factors (Bojesen et al., 2013; Codd et al., 2013; Gu et al., 2011) but also by nongenetic factors through an effect on oxidative stress and inflammation, the major causes of accelerated telomere erosion (Kawanishi and Oikawa, 2004; O'Donovan et al., 2011; Saretzki and Von Zglinicki, 2002). Non-genetic factors affecting TL include smoking (Nawrot et al., 2010), socioeconomic status and physical activity (Cherkas et al., 2008), marine omega-3 fatty acid intake (Farzaneh-Far et al., 2010), psychological stressors (Damjanovic et al., 2007; Epel et al., 2004; Lansdorp, 2006), and obesity (Buxton et al., 2011; Lee et al., 2011; Njajou et al., 2012). Furthermore, twin studies indicate that nongenetic factors may have significant effects on TL later in life (Cherkas et al., 2008; Huda et al., 2007), suggesting that although TL is inheritable (Codd et al., 2010; Njajou et al., 2010; O'Donovan et al., 2011; Vasa-Nicotera et al., 2005), environmental influences play a key role in modulating the rate of telomere shortening. "
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    ABSTRACT: Centenarians and their offspring are increasingly considered a useful model to study and characterize the mechanisms underlying healthy aging and longevity. The aim of this project is to compare the prevalence of age-related diseases and telomere length (TL), a marker of biological age and mortality, across five groups of subjects: semisupercentenarians (SSCENT) (105-109years old), centenarians (CENT) (100-104years old), centenarians' offspring (CO), age- and gender-matched offspring of parents who both died at an age in line with life expectancy (CT) and age- and gender-matched offspring of both non-long-lived parents (NLO). Information was collected on lifestyle, past and current diseases, medical history and medication use. SSCENT displayed a lower prevalence of acute myocardial infarction (p=0.027), angina (p=0.016) and depression (p=0.021) relative to CENT. CO appeared to be healthier compared to CT who, in turn, displayed a lower prevalence of both arrhythmia (p=0.034) and hypertension (p=0.046) than NLO, characterized by the lowest parental longevity. Interestingly, CO and SSCENT exhibited the longest (p<0.001) and the shortest (p<0.001) telomeres respectively while CENT showed no difference in TL compared to the younger CT and NLO. Our results strengthen the hypothesis that the longevity of parents may influence the health status of their offspring. Moreover, our data also suggest that both CENT and their offspring may be characterized by a better TL maintenance which, in turn, may contribute to their longevity and healthy aging. The observation that SSCENT showed considerable shorter telomeres compared to CENT may suggest a progressive impairment of TL maintenance mechanisms over the transition from centenarian to semisupercentenarian age.
    Experimental Gerontology 06/2014; 58. DOI:10.1016/j.exger.2014.06.018 · 3.49 Impact Factor
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