Presence of low-grade inflammation impaired postprandial stimulation of muscle protein synthesis in old rats
Presence of low-grade inflammation impaired postprandial stimulation of muscle protein synthesis in old rats
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DOI：
10.1016/j.jnutbio.2009.01.005
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发表时间：
2010-04-01
影响因子：
5.6
通讯作者：
Dardevet, Dominique
中科院分区：
文献类型：
--
作者：
Balage, Michele;Averous, Julien;Dardevet, Dominique
衰老的特征是肌肉质量下降，这可以解释为餐后肌肉蛋白质代谢调节的缺陷。本研究旨在探讨老年人低度炎症（LGI）的发生与肌肉蛋白质合成和降解途径对食物摄入的抵抗之间可能存在的联系。对55只20月龄大鼠进行了为期5个月的研究;每月抽血一次，以评估血浆纤维蛋白原和α 2-巨球蛋白。然后在25月龄时根据它们的炎症状态将动物分成两组：对照非炎症组（NI，n=24）和低度炎症组（LGI，n=23）。实验当天，大鼠没有进食或进食。肌肉蛋白质合成在体内评估使用泛剂量法（[1-C-13]苯丙氨酸）和蛋白质S6激酶的肌肉磷酸化，并在腓肠肌中测量蛋白质S6。肌肉蛋白水解进行了评估，在体外使用的上棘肌。NI和LGI的吸收后肌肉蛋白质合成和蛋白质水解相似。进食后，肌肉蛋白质的合成显着刺激NI，但仍然在LGI反应迟钝。无论炎症和/或营养状况如何，两组的肌肉蛋白水解相似。总之。我们发现，在衰老过程中LGI的发展可能是，至少部分是，由食物摄入诱导的大鼠肌肉蛋白质合成刺激缺陷的原因。我们的研究结果表明，控制老年人LGI的发展，改善膳食对肌肉蛋白质合成的影响，从而减缓肌肉减少症。(C)2010年爱思唯尔公司All rights reserved.
Aging is characterized by a decline in muscle mass that could be explained by a defect in the regulation of postprandial muscle protein metabolism. This study was undertaken to examine a possible link between the development of low-grade inflammation (LGI) in elderly and the resistance of muscle protein synthesis and degradation pathways to food intake. Fifty-five 20-month-old-rats were studied for 5 months; blood was withdrawn once a month to assess plasma fibrinogen and alpha 2-macroglobulin. Animals were then separated into two groups at 25 months old according to their inflammation status: a control non-inflamed (NI, n=24) and a low-grade inflamed group (LGI, n=23). The day of the experiment, rats received no food or a meal. Muscle protein synthesis was assessed in vivo using the flooding dose method ([1-C-13]phenylalanine) and muscle phosphorylation of protein S6 kinase, and protein S6 was measured in gastrocnemius muscle. Muscle proteolysis was assessed in vitro using the epitrachlearis muscle. Postabsorptive muscle protein synthesis and proteolysis were similar in NI and LGI. After food intake, muscle protein synthesis was significantly stimulated in NI but remained unresponsive in LGI. Muscle proteolysis was similar in both groups whatever the inflammation and/or the nutritional status. In conclusion. we showed that development of LGI during aging may be responsible, at least in part, for the defect in muscle protein synthesis stimulation induced by food intake in rats. Our results suggested that the control of LGI development in elderly improve meal effect on muscle protein synthesis and consequently slow down sarcopenia. (C) 2010 Elsevier Inc. All rights reserved.