Sarcopenic obesity is associated with telomere shortening: findings from the NHANES 1999\u20132002

Thomas Goddard,Kostas Tsintzas,Mario Siervo,Carla M Prado,Mohsen Mazidi,Blossom C M Stephan

doi:10.1038/s41366-021-00995-z

Abstract

Sarcopenic obesity (SO) is characterised by the concurrent presence of sarcopenia and excess adiposity. Telomere shortening has been associated with sarcopenia and obesity alone but the association between SO and telomere length (TL) has not been investigated. This study aimed to investigate SO and TL in an adult population. Data were from 5397 individuals (mean age = 44.7 years, 51.3% male) enrolled in the National Health and Nutrition Examination Survey. Body composition (BC) was assessed by Dual Energy X-Ray Absorptiometry. Two models were used to assess SO: a BC model including four phenotypes derived from the combination of high or low adiposity and muscle mass; and, a truncal fat mass to appendicular skeletal mass ratio (TrFM/ASM). TL was assessed using quantitative polymerase chain reaction and expressed as base pairs. The mean TL, relative to the reference DNA, was calculated and expressed as the mean T/S ratio. A General Linear Model was applied to determine associations between TL for SO. In adjusted analysis, only individuals with SO, defined as the presence of high adiposity-low muscle mass (four-phenotype model), had significantly shorter telomeres (p = 0.05) than the reference group (i.e. low adiposity-high muscle mass), with a mean T/S ratio of 1.02 (95%CI: 0.98–1.05) compared to 1.05 (95%CI: 1.01–1.09), respectively. TrFM/ASM was not associated with TL. Preliminary findings suggest that sarcopenia and obesity may act synergistically to shorten telomeres.

Highlights

Sarcopenic obesity (SO) is defined by the concurrent presence of low muscle mass and high adiposity [1]
No significant association was found between truncal fat mass (TrFM)/appendicular skeletal muscle mass (ASM) phenotypes and telomere length (TL), or between body mass index (BMI) groups and TL (Table 2). These preliminary results suggest that SO may be associated with telomere shortening and may represent an important risk factor for accelerated ageing than sarcopenia and obesity alone
The TrFM/ASM model found no significant association between SO and TL; this result was unexpected as truncal fat accumulation has been associated with greater impairment of cardio-metabolic health [10]

Summary

Introduction

Sarcopenic obesity (SO) is defined by the concurrent presence of low muscle mass (sarcopenia) and high adiposity (obesity) [1]. SO appears to confer a greater risk for cardio-metabolic diseases and mortality, than either sarcopenia or obesity alone [1]. In the absence of sufficient telomerase activity, telomeres are shortened, and this has been used as a biomarker of biological ageing [2]. Individuals with shorter telomeres may have a greater risk of cardiometabolic disorders and mortality [2]. Even though telomere shortening has been associated with sarcopenia and obesity separately [3, 4], the link between SO and telomere length (TL) has not been investigated to determine whether SO may represent a greater risk factor for accelerated ageing and agerelated cardio-metabolic disorders

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Conclusion