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Glutamine-stimulated in vitro hypertrophy is preserved in muscle cells from older women.
Mechanisms of Ageing and Development ( IF 5.3 ) Pub Date : 2020-03-03 , DOI: 10.1016/j.mad.2020.111228
Thomas Chaillou 1 , Igor Sanna 1 , Fawzi Kadi 1
Affiliation  

Age-related loss of muscle mass may result from reduced protein synthesis stimulation in response to anabolic stimuli, such as amino acid (AA) supplementation. The exact etiology of anabolic resistance to AA remains unclear. Therefore, the aim of this study was to investigate the anabolic response [cell size, protein synthesis and mechanistic target of rapamycin (mTOR) pathway] to the AA glutamine (a strong anabolic AA highly present in skeletal muscle) in myotubes obtained from 8 young (YW; 21-35 yrs) and 8 older (OW; 65-70 yrs) healthy women. This in vitro model of human primary myogenic cells explores the intrinsic behavior of muscle cells, while excluding potential influences of external factors. We showed that despite lower muscle mass, strength and cardiorespiratory fitness in OW compared to YW, myotube size (myotube diameter and area) and protein synthesis were not altered in OW, and glutamine-induced myotube hypertrophy and protein synthesis were preserved in OW. Apart from a lower glutamine-induced increase in P70S6 kinase phosphorylation in OW, no significant differences in other components of the mTOR pathway were observed between groups. Altogether, our data support the idea that the intrinsic capacity of muscle cells to respond to glutamine stimulation is preserved in healthy older women.

中文翻译:

谷氨酰胺刺激的体外肥大保留在老年妇女的肌肉细胞中。

与年龄相关的肌肉质量损失可能是由于响应合成代谢刺激(例如氨基酸(AA)补充)而减少的蛋白质合成刺激导致的。对AA的合成代谢抗性的确切病因仍不清楚。因此,本研究的目的是研究从8位年轻人获得的肌管中对AA谷氨酰胺(骨骼肌中高度存在的强合成代谢AA)的合成代谢反应[细胞大小,蛋白质合成和雷帕霉素(mTOR)通路的机制靶点]。 (YW; 21-35岁)和8位年龄较大(OW; 65-70岁)的健康女性。这种人类原代成肌细胞的体外模型探索了肌肉细胞的内在行为,同时排除了外部因素的潜在影响。我们发现,尽管与YW相比,OW的肌肉质量,力量和心肺适应性较低,OW中肌管大小(肌管直径和面积)和蛋白质合成没有改变,谷氨酰胺诱导的肌管肥大和蛋白质合成在OW中得以保留。除了在OW中较低的谷氨酰胺诱导的P70S6激酶磷酸化增加外,两组之间未观察到mTOR途径的其他成分的显着差异。总之,我们的数据支持这样的观点,即健康的老年妇女保留了肌细胞对谷氨酰胺刺激作出反应的内在能力。
更新日期:2020-03-03
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