Roubenoff Ronenn
Department of Molecular Medicine, Millennium Pharmaceuticals Inc, Cambridge, Massachusetts 02139, USA.
Curr Opin Clin Nutr Metab Care. 2003 May;6(3):295-9. doi: 10.1097/01.mco.0000068965.34812.62.
Research in the field of sarcopenia is evolving rapidly, and the process is now recognized as an important cause of frailty and morbidity in the elderly. This review focuses on recent developments in the field, especially regarding the role of catabolic stimuli in causing sarcopenia.
There is now an impressive body of literature implicating increased interleukin-6 levels in successfully aging adults. New data indicate that high interleukin-6 levels carry a poor prognosis, although it is not clear if the cytokine has primarily a causal or counter-regulatory function. Interleukin-6 and other cytokines could function through direct catabolic effects, or by causing reduced dietary energy intake (the anorexia of aging), or by inducing insulin resistance or lowering growth hormone-insulin-like growth factor-I concentrations. Furthermore, apoptosis has now been linked to sarcopenia, suggesting that an inflammatory signal could trigger loss of muscle cells in the elderly even in the absence of overt inflammatory disease.
Aging causes loss of many of the anabolic signals to muscle that are present in young adulthood. Recent research suggests that there is also an increase in catabolic signals with age.
肌肉减少症领域的研究发展迅速，该过程目前被认为是老年人虚弱和发病的重要原因。本综述聚焦于该领域的最新进展，尤其是分解代谢刺激在导致肌肉减少症中的作用。
目前有大量文献表明，成功衰老的成年人白细胞介素-6水平升高。新数据表明，高白细胞介素-6水平预后较差，尽管尚不清楚该细胞因子主要具有因果作用还是反调节功能。白细胞介素-6和其他细胞因子可能通过直接分解代谢作用发挥功能，或通过导致饮食能量摄入减少（衰老性厌食），或通过诱导胰岛素抵抗或降低生长激素-胰岛素样生长因子-I浓度发挥作用。此外，细胞凋亡现已与肌肉减少症相关联，这表明即使在没有明显炎症性疾病的情况下，炎症信号也可能触发老年人肌肉细胞的丧失。
衰老导致许多在年轻时存在的对肌肉的合成代谢信号丧失。最近的研究表明，随着年龄增长，分解代谢信号也会增加。
