Department of Psychosomatic Internal Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
Int J Biochem Cell Biol. 2013 Oct;45(10):2179-85. doi: 10.1016/j.biocel.2013.07.016. Epub 2013 Jul 30.
Cachexia is characterized by anorexia, weakness, weight loss, and muscle wasting. Anorexia and muscle wasting are the key features of cachexia and they affect mortality, morbidity, and quality of life. Consistent studies have found that feeding-regulating peptides such as melanocortin, ghrelin, and leptin are related to muscle metabolism, and the balance of catabolism and anabolism in muscle is regulated in the hypothalamus, which also regulates appetite and energy expenditure. In cachexia, proinflammatory cytokines, such as TNF-α, IL-1, IL-6 and Angiotensin II induce muscle atrophy. The mechanism is suggested via upregulation of MuRF1 and MAFbx. In contrast, the orexigenic peptide, AgRP and ghrelin have the effect to decrease proinflammatory cytokines and increase body weight, food intake, and muscle mass. The understandings of the pathological mechanism of anorexia and muscle metabolism in view of the crosstalk between brain and muscle will open the new way for the management of cachexia. In this review, we describe recent experimental and clinical studies that have examined the regulation of food intake and muscle wasting in cachexia. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.
恶病质的特征为厌食、虚弱、体重减轻和肌肉萎缩。厌食和肌肉萎缩是恶病质的关键特征，它们影响死亡率、发病率和生活质量。一致的研究发现，调节进食的肽类如黑素细胞刺激素、胃饥饿素和瘦素与肌肉代谢有关，肌肉的分解代谢和合成代谢平衡在调节食欲和能量消耗的下丘脑受到调节。在恶病质中，促炎细胞因子如 TNF-α、IL-1、IL-6 和血管紧张素 II 诱导肌肉萎缩。其机制被认为是通过上调 MuRF1 和 MAFbx 来实现的。相反，食欲肽 AgRP 和胃饥饿素具有降低促炎细胞因子和增加体重、食物摄入和肌肉质量的作用。鉴于大脑和肌肉之间的相互作用，对厌食和肌肉代谢的病理机制的理解将为恶病质的管理开辟新的途径。在这篇综述中，我们描述了最近的实验和临床研究，这些研究检查了恶病质中食物摄入和肌肉消耗的调节。本文是题为“肌肉消耗的分子基础”的专题的一部分。
