Epigenomics · 2026
Accelerated epigenetic aging and shorter DNA methylation-based telomere length in sarcopenic obesity: an exploratory pilot study.
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Rossini Venturini Ana Claudia, Fogagnolo Caroline, Ortiz Gabriela Ueta, da Silva Rodrigues Guilherme, da Silva Arthur Polveiro, Noronha Natália Yumi, Abud Gabriela Ferreira, Silva Bianca Monteiro, Benzoni Gabriela Geraldo, de Souza Pinhel Marcela Augusta, Watanabe Lígia Moriguchi, Sae-Lee Chanachai, Travieso Sofia Germano, de Lima Viliod Marcela Coffacci, Nonino Carla Barbosa, da Silva Adelino Sanchez Ramos, de Freitas Ellen Cristini
Аннотация
BACKGROUND: Sarcopenic obesity (SO), defined as the coexistence of excess fat mass and low muscle mass/function, has been linked to adverse outcomes. Epigenetic alterations are central hallmarks of aging. Evaluating how obesity, sarcopenia, and SO are related to epigenetic aging biomarkers may provide insights into cellular aging and disease risk.
METHODS: In this cross-sectional study, 30 older women were classified into the control, obesity, sarcopenia, and SO groups and underwent anthropometry measurements, body composition analysis, and handgrip strength. Blood DNA methylation (DNAm) biomarkers were used to estimate eight epigenetic clocks (Horvath, Hannum, DNAmTL, PhenoAge, GrimAge, GrimAge2, Zhang, and FitAge) and to calculate intrinsic and extrinsic epigenetic age acceleration (IEAA and EEAA). Associations were tested with Bayesian linear and quantile regressions, adjusted for age and HOMA-IR.
RESULTS: SO was associated with higher EEAA, DNAmFitAge, and Hannum clock estimates, and shorter DNAmTL in both models. Obesity showed positive associations with these clocks in adjusted models and higher quantiles.
CONCLUSIONS: SO is associated with accelerated aging and shorter DNAmTL. Obesity contributes to biological aging, whereas sarcopenia without obesity does not. These findings suggest that excess adiposity combined with low muscle mass may worsen age-related decline, although the small sample size should be considered.
METHODS: In this cross-sectional study, 30 older women were classified into the control, obesity, sarcopenia, and SO groups and underwent anthropometry measurements, body composition analysis, and handgrip strength. Blood DNA methylation (DNAm) biomarkers were used to estimate eight epigenetic clocks (Horvath, Hannum, DNAmTL, PhenoAge, GrimAge, GrimAge2, Zhang, and FitAge) and to calculate intrinsic and extrinsic epigenetic age acceleration (IEAA and EEAA). Associations were tested with Bayesian linear and quantile regressions, adjusted for age and HOMA-IR.
RESULTS: SO was associated with higher EEAA, DNAmFitAge, and Hannum clock estimates, and shorter DNAmTL in both models. Obesity showed positive associations with these clocks in adjusted models and higher quantiles.
CONCLUSIONS: SO is associated with accelerated aging and shorter DNAmTL. Obesity contributes to biological aging, whereas sarcopenia without obesity does not. These findings suggest that excess adiposity combined with low muscle mass may worsen age-related decline, although the small sample size should be considered.