Egawa Tatsuro, Tsuda Satoshi, Goto Ayumi, Ohno Yoshitaka, Yokoyama Shingo, Goto Katsumasa, Hayashi Tatsuya
1Laboratory of Sports and Exercise Medicine,Graduate School of Human and Environmental Studies,Kyoto University,Kyoto,606-8501,Japan.
3Laboratory of Physiology,School of Health Sciences,Toyohashi Sozo University,Toyohashi,Aichi,440-8511,Japan.
Br J Nutr. 2017 Jan;117(1):21-29. doi: 10.1017/S0007114516004591. Epub 2017 Jan 17.
Diets enriched with advanced glycation end products (AGE) have recently been related to muscle dysfunction processes. However, it remains unclear whether long-term exposure to an AGE-enriched diet impacts physiological characteristics of skeletal muscles. Therefore, we explored the differences in skeletal muscle mass, contractile function and molecular responses between mice receiving a diet high in AGE (H-AGE) and low in AGE (L-AGE) for 16 weeks. There were no significant differences between L-AGE and H-AGE mice with regard to body weight, food intake or epididymal fat pad weight. However, extensor digitorum longus (EDL) and plantaris (PLA) muscle weights in H-AGE mice were lower compared with L-AGE mice. Higher levels of N ε -(carboxymethyl)-l-lysine, a marker for AGE, in EDL muscles of H-AGE mice were observed compared with L-AGE mice. H-AGE mice showed lower muscle strength and endurance in vivo and lower muscle force production of PLA muscle in vitro. mRNA expression levels of myogenic factors including myogenic factor 5 and myogenic differentiation in EDL muscle were lower in H-AGE mice compared with L-AGE mice. The phosphorylation status of 70-kDa ribosomal protein S6 kinase Thr389, an indicator of protein synthesis signalling, was lower in EDL muscle of H-AGE mice than that of L-AGE mice. These findings suggest that long-term exposure to an AGE-enriched diet impairs skeletal muscle growth and muscle contractile function, and that these muscle dysfunctions may be attributed to the inhibition of myogenic potential and protein synthesis.
富含晚期糖基化终末产物（AGE）的饮食最近被认为与肌肉功能障碍过程有关。然而，长期暴露于富含AGE的饮食是否会影响骨骼肌的生理特性仍不清楚。因此，我们探究了接受富含AGE的高糖饮食（H-AGE）和低糖饮食（L-AGE）16周的小鼠在骨骼肌质量、收缩功能和分子反应方面的差异。L-AGE组和H-AGE组小鼠在体重、食物摄入量或附睾脂肪垫重量方面没有显著差异。然而，与L-AGE组小鼠相比，H-AGE组小鼠的趾长伸肌（EDL）和跖肌（PLA）重量更低。与L-AGE组小鼠相比，在H-AGE组小鼠的EDL肌肉中观察到更高水平的AGE标志物Nε-（羧甲基）-L-赖氨酸。H-AGE组小鼠在体内表现出较低的肌肉力量和耐力，在体外PLA肌肉产生的力量也较低。与L-AGE组小鼠相比，H-AGE组小鼠EDL肌肉中包括生肌因子5和成肌分化在内的生肌因子mRNA表达水平更低。70 kDa核糖体蛋白S6激酶Thr389的磷酸化状态是蛋白质合成信号的一个指标，H-AGE组小鼠EDL肌肉中的该指标低于L-AGE组小鼠。这些发现表明，长期暴露于富含AGE的饮食会损害骨骼肌生长和肌肉收缩功能，并且这些肌肉功能障碍可能归因于生肌潜能和蛋白质合成的抑制。
