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合成代谢信号缺陷是消瘦、衰老肌肉对氨基酸产生抗性的基础。

Anabolic signaling deficits underlie amino acid resistance of wasting, aging muscle.

作者信息

Cuthbertson Daniel, Smith Kenneth, Babraj John, Leese Graham, Waddell Tom, Atherton Philip, Wackerhage Henning, Taylor Peter M, Rennie Michael J

机构信息

Division of Molecular Physiology, School of Life Sciences, University of Dundee, Dundee, Scotland.

出版信息

FASEB J. 2005 Mar;19(3):422-4. doi: 10.1096/fj.04-2640fje. Epub 2004 Dec 13.

Abstract

The nature of the deficit underlying age-related muscle wasting remains controversial. To test whether it could be due to a poor anabolic response to dietary amino acids, we measured the rates of myofibrillar and sarcoplasmic muscle protein synthesis (MPS) in 44 healthy young and old men, of similar body build, after ingesting different amounts of essential amino acids (EAA). Basal rates of MPS were indistinguishable, but the elderly showed less anabolic sensitivity and responsiveness of MPS to EAA, possibly due to decreased intramuscular expression, and activation (phosphorylation) after EAA, of amino acid sensing/signaling proteins (mammalian target of rapamycin, mTOR; p70 S6 kinase, or p70(S6k); eukaryotic initiation factor [eIF]4BP-1; and eIF2B). The effects were independent of insulin signaling since plasma insulin was clamped at basal values. Associated with the anabolic deficits were marked increases in NFkappaB, the inflammation-associated transcription factor. These results demonstrate first, EAA stimulate MPS independently of increased insulin availability; second, in the elderly, a deficit in MPS in the basal state is unlikely; and third, the decreased sensitivity and responsiveness of MPS to EAA, associated with decrements in the expression and activation of components of anabolic signaling pathways, are probably major contributors to the failure of muscle maintenance in the elderly. Countermeasures to maximize muscle maintenance should target these deficits.

摘要

与年龄相关的肌肉萎缩背后的缺陷本质仍存在争议。为了测试其是否可能是由于对膳食氨基酸的合成代谢反应不佳,我们在摄入不同量的必需氨基酸(EAA)后,测量了44名体型相似的健康年轻男性和老年男性的肌原纤维和肌浆蛋白合成(MPS)速率。MPS的基础速率没有差异,但老年人对EAA的MPS合成代谢敏感性和反应性较低,这可能是由于氨基酸感应/信号蛋白(雷帕霉素哺乳动物靶蛋白,mTOR;p70 S6激酶,或p70(S6k);真核起始因子[eIF]4BP-1;和eIF2B)的肌肉内表达和EAA后的激活(磷酸化)降低所致。这些影响与胰岛素信号无关,因为血浆胰岛素被钳制在基础值。与合成代谢缺陷相关的是炎症相关转录因子NFkappaB的显著增加。这些结果首先表明,EAA独立于胰岛素可用性增加而刺激MPS;其次,在老年人中,基础状态下MPS缺乏不太可能;第三,MPS对EAA的敏感性和反应性降低,与合成代谢信号通路成分的表达和激活减少有关,可能是老年人肌肉维持失败的主要原因。最大化肌肉维持的对策应针对这些缺陷。

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