Abstract

In patients with chronic kidney disease, sarcopenia is associated with decreased renal function and correlates with increased morbidity and mortality. Although the molecular mechanism to underlie uremic sarcopenia is not fully elucidated yet, accumulation of uremic toxin might exert a direct negative effect on skeletal muscle via reactive oxygen species (ROS) and mitochondrial dysfunction. For livestock, β2-adrenergic receptor (β2-AR) agonists are allegedly used in anticipation of ergogenic effect, which brought to us a hypothesis that the drug could be promising to ameliorate skeletal muscle mass reduction and dysfunction of uremic sarcopenia.

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