Reveals metabolic disruption drives sarcopenia and frailty in aging and chronic kidney disease, suggesting important connections.
Metabolic imbalance is a key driver of senescence. Renal proximal tubular cells possess intrinsic gluconeogenic capacity, and its loss has been reported in chronic kidney disease (CKD), although systemic effects remain unclear. CKD promotes multisystem aging and frailty and is considered a model of premature aging. We hypothesized that renal metabolic decline disrupts systemic glucose homeostasis and accelerates senescence. Sarcopenia, an aging-related disorder, is strongly associated with CKD, yet young CKD mice rarely show muscle atrophy.
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KOJIMA et al. (2026) studied this question.
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