Abstract
Prevalence of sarcopenia is high in patients with chronic kidney disease (CKD), especially in those with dialysis. Various pathological conditions related to CKD, such as chronic inflammation, insulin resistance, and endothelial dysfunction, are thought to be associated with the development and progression of sarcopenia. Advanced glycation end products (AGE), one of the representative uremic toxins, have been shown to contribute to various CKD-associated complications. This study investigated the role of AGE in frailty and sarcopenia in patients and animals with CKD, respectively. In patients undergoing dialysis, serum AGE levels were significantly increased according to the frailty status and inversely associated with physical performance and activity. AGE accumulated in the gastrocnemius muscle of 5/6 nephrectomy mice in association with morphological abnormalities, capillary rarefaction, and mitochondrial dysfunction, all of which were completely inhibited by DNA-aptamer raised against AGE. Our present findings may suggest the pathological role of AGE in sarcopenia and frailty in CKD.
Highlights
Prevalence of sarcopenia is high in patients with chronic kidney disease (CKD), especially in those with dialysis
When Advanced glycation end products (AGE) levels were stratified by the frailty status, serum levels of AGE were significantly increased according to the degree of frailty (p = 0.02, by analysis of variance (ANOVA)) (Fig. 1)
The present findings were consistent with the previous observations in older community-dwelling adults showing that elevated serum AGE levels were associated with slow walking s peed[21]
Summary
Prevalence of sarcopenia is high in patients with chronic kidney disease (CKD), especially in those with dialysis. CKD was originally known as one of the representative conditions that could accelerate premature a ging[6], and various pathological conditions associated with CKD, such as chronic inflammation, insulin resistance, and increased uremic toxins, have been shown to contribute to the risk of aging-related disorders, including sarcopenia and frailty[3,7,8]. An in vitro-study revealed that AGE could induce muscle atrophy and impair myogenesis via a RAGE-mediated signaling pathway[24] These observations led us to hypothesize that accumulation of AGE in CKD, one of the representative diseases that accelerate aging-related disorders, Scientific Reports | (2020) 10:17647. We investigated the pathological role of AGE in frailty and sarcopenia in CKD patients and an animal model of CKD, respectively
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