Association of advanced glycation end products with sarcopenia and frailty in chronic kidney disease

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作者
Junko Yabuuchi
Seiji Ueda
Sho-ichi Yamagishi
Nao Nohara
Hajime Nagasawa
Keiichi Wakabayashi
Takanori Matsui
Higashimoto Yuichiro
Tomoyasu Kadoguchi
Tomoyuki Otsuka
Tomohito Gohda
Yusuke Suzuki
机构
[1] Juntendo University Faculty of Medicine,Department of Nephrology
[2] Showa University School of Medicine,Division of Diabetes, Metabolism and Endocrinology, Department of Medicine
[3] Kurume University School of Medicine,Department of Pathophysiology and Therapeutics of Diabetic Vascular Complications
[4] Kurume University School of Medicine,Department of Chemistry
[5] Juntendo University Graduate School of Medicine,Department of Cardiovascular Medicine
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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.
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