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首页> 外文期刊>Current opinion in gastroenterology >Cancer cachexia.
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Cancer cachexia.

机译：癌症恶病质。

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PURPOSE OF REVIEW: Although cachexia has a major effect on both the morbidity and mortality of cancer patients, information on the mechanisms responsible for this condition is limited. This review summarizes recent data in this area. RECENT FINDINGS: Cachexia is defined as loss of muscle, with or without fat, frequently associated with anorexia, inflammation and insulin resistance. Loss of adipose mass is due to an increased lipolysis through an increased expression of hormone-sensitive lipase. Adipose tissue does not contribute to the inflammatory response. There is an increased phosphorylation of both protein kinase R (PKR) and eukaryotic initiation factor 2 on the alpha-subunit in skeletal muscle of cachectic cancer patients, which would lead to muscle atrophy through a depression in protein synthesis and an increase in degradation. Mice lacking the ubiquitin ligase MuRF1 are less susceptible to muscle wasting under amino acid deprivation. Expression of MuRF1 and atrogin-1 is increased by oxidative stress, whereas nitric oxide may protect against muscle atrophy. Levels of interleukin (IL)-6 correlate with cachexia and death due to an increase in tumour burden. Ghrelin analogues and melanocortin receptor antagonists increase food intake and may have a role in the treatment of cachexia. SUMMARY: These findings provide impetus for the development of new therapeutic agents.
机译：审查的目的：尽管恶病质对癌症患者的发病率和死亡率都有重大影响，但有关造成这种情况的机制的信息有限。这篇综述总结了这方面的最新数据。最新发现：恶病质定义为肌肉丢失，有脂肪或无脂肪，经常与厌食症，炎症和胰岛素抵抗相关。脂肪量的损失归因于激素敏感性脂肪酶表达的增加，脂肪分解增加。脂肪组织不会促进炎症反应。恶病质癌症患者骨骼肌中的α-亚基上的蛋白激酶R（PKR）和真核起始因子2的磷酸化增加，这将通过蛋白质合成降低和降解增加而导致肌肉萎缩。缺乏泛素连接酶MuRF1的小鼠在氨基酸剥夺下更不容易消耗肌肉。氧化应激可增加MuRF1和atrogin-1的表达，而一氧化氮可预防肌肉萎缩。白细胞介素（IL）-6的水平与恶病质和因肿瘤负担增加而导致的死亡相关。生长激素释放肽类似物和黑皮质素受体拮抗剂可增加食物摄入，并可能在恶病质的治疗中发挥作用。概述：这些发现为新型治疗剂的开发提供了动力。

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