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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Sarcopenia is characterized by the progressive loss of skeletal muscle mass and strength with aging. In patients with chronic kidney disease (CKD), sarcopenia frequently coexists and worsens physical frailty and mortality, especially among the elderly. However, preventive or therapeutic strategies for CKD-associated sarcopenia remain undefined. We have previously reported that uremic toxins accumulate not only in the circulation but also within skeletal muscle, contributing to muscle wasting. Yet, the detailed metabolic alterations underlying CKD-associated sarcopenia remain unclear. Skeletal muscles differ in metabolic phenotype—fast-twitch (glycolytic; type II), slow-twitch (oxidative; type I), and mixed fibers—and aging-related sarcopenia mainly affects type II fibers, whereas CKD-associated sarcopenia may involve a glycolytic shift. This study aimed to elucidate age- and fiber type–specific metabolic remodeling in CKD-associated sarcopenia using comprehensive metabolomic profiling.
Male C57BL/6 mice aged 8 weeks (young) or 25 weeks (adult) were fed either control chow or chow containing 0.2% adenine for 6 weeks to induce CKD. Skeletal muscles—extensor digitorum longus (EDL; fast-twitch), soleus (SOL; slow-twitch), and gastrocnemius (GAS; mixed) were collected. Muscle metabolites were extracted using a water/methanol/chloroform mixture, derivatized by methoximation and trimethylsilylation, and analyzed using GC-MS (GCMS-TQ8040, Shimadzu) with the Smart Metabolites Database based multiple reaction monitoring method. Data were processed and statistically analyzed using MetaboAnalyst 6.0.
All CKD groups exhibited significant decreases in muscle mass in EDL, SOL, and GAS. Enrichment analysis identified hypotaurine as the most markedly decreased metabolite across all CKD groups. In taurine–hypotaurine metabolism, hypotaurine and cysteine levels were reduced in all muscles of young CKD mice, whereas taurine levels paradoxically increased. In contrast, adult CKD mice showed significant reductions in hypotaurine without taurine recovery. In purine metabolism, adenosine, inosine, hypoxanthine, and xanthine were significantly elevated only in the EDL of young CKD mice. Taurine and adenosine, both known for antioxidant and cytoprotective effects, were increased exclusively in young CKD muscles, suggesting age-dependent adaptive responses against uremic stress.
Comprehensive metabolomic profiling revealed distinct, age- and fiber type–specific metabolic changes in CKD-associated sarcopenia. Younger CKD muscles exhibit compensatory activation of antioxidant and purine metabolic pathways, whereas adult muscles fail to mount such adaptive responses, potentially accelerating sarcopenic progression. These findings provide novel insights into metabolic remodeling that underlies muscle fragility in CKD and may guide future strategies to prevent or treat CKD-related sarcopenia.
