Diabetes research and clinical practice · 2026
Telomere length as a biomarker of early cumulative burden of metabolic syndrome components.
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Millán Andrea Liliana, Rojo Mailén, Duarte Alejandra, Pérez Hernán, López Ariel Pablo, Frechtel Gustavo Daniel
Аннотация
AIMS: This study evaluated telomere length (TL) as a biomarker of cumulative metabolic dysfunction. We assessed the association between TL and Metabolic Syndrome (MS), its individual components, and their clustering, while comparing obesity phenotypes to evaluate TL's utility in stratifying biological risk during the transition to metabolic impairment.
METHODS: In 331 participants, TL was measured by qPCR. Associations were analyzed using three incremental linear regression models (unadjusted, age/sex-adjusted, and fully adjusted). TL was compared across three groups: Normal Weight (NW0), Metabolically Healthy Obesity (MHO), and Obesity with MS (OMS).
RESULTS: MS diagnosis was robustly associated with shorter TL in the fully adjusted model (p < 0.001). Central adiposity and dyslipidemia were the primary drivers of attrition. A non-linear pattern emerged regarding cumulative burden of MS components: TL significantly shortened with the first three components but showed no further reduction with four or five. TL was different between phenotypes; MHO subjects exhibited significantly shorter TL than NW0 (p = 0.005) but longer than OMS group (p = 0.025).
CONCLUSIONS: The non-linear pattern of attrition and differences in TL across NW0, MHO, and OSM phenotypes suggest that TL captures the systemic biological impact of metabolic clustering rather than the additive effect of individual risk factors.
METHODS: In 331 participants, TL was measured by qPCR. Associations were analyzed using three incremental linear regression models (unadjusted, age/sex-adjusted, and fully adjusted). TL was compared across three groups: Normal Weight (NW0), Metabolically Healthy Obesity (MHO), and Obesity with MS (OMS).
RESULTS: MS diagnosis was robustly associated with shorter TL in the fully adjusted model (p < 0.001). Central adiposity and dyslipidemia were the primary drivers of attrition. A non-linear pattern emerged regarding cumulative burden of MS components: TL significantly shortened with the first three components but showed no further reduction with four or five. TL was different between phenotypes; MHO subjects exhibited significantly shorter TL than NW0 (p = 0.005) but longer than OMS group (p = 0.025).
CONCLUSIONS: The non-linear pattern of attrition and differences in TL across NW0, MHO, and OSM phenotypes suggest that TL captures the systemic biological impact of metabolic clustering rather than the additive effect of individual risk factors.