l-Lysine suppresses myofibrillar protein degradation and autophagy in skeletal muscles of senescence-accelerated mouse prone 8

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• 作者：Tomonori Sato ; Yoshiaki Ito ; Takashi Nagasawa
• 关键词：Sarcopenia ; Autophagy ; Ubiquitin proteasome system ; Skeletal muscle ; Lysine
• 刊名：Biogerontology
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：18
• 期：1
• 页码：85-95
• 全文大小：
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Cell Biology; Geriatrics/Gerontology; Developmental Biology;
• 出版者：Springer Netherlands
• ISSN：1573-6768
• 卷排序：18

文摘

Sarcopenia is a condition of the loss of muscle mass that is associated with aging and that increases the risk for bedridden state, thereby warranting studies of interventions that attenuate sarcopenia. Here the effects of 2-month dietary l-lysine (Lys) supplementation (1.5–3.0 %) on myofibrillar protein degradation and major proteolytic systems were investigated in senescence-accelerated mouse prone 8 (SAMP8). At 36 weeks of age, skeletal muscle and lean body mass was reduced in SAMP8 when compared with control senescence-accelerated mouse resistant 1 (SAMR1). The myofibrillar protein degradation, which was evaluated by the release of 3-methylhistidine, was stimulated in SAMP8, and the autophagy activity, which was evaluated by light chain 3-II, was stimulated in the skeletal muscle of SAMP8. The activation of ubiquitin-proteasome system was not observed in the muscles of SAMP8. However, myofibrillar protein degradation and autophagic activity in skeletal muscles of SAMP8 were suppressed by dietary intake of 3.0 % Lys. The present data indicate that myofibrillar protein degradation by bulk autophagy is stimulated in the skeletal muscles of SAMP8 and that dietary Lys supplementation attenuates sarcopenia in SAMP8 by suppressing autophagic proteolysis.