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对厌食作为患有肉瘤的非生长小鼠骨骼肌中蛋白质合成改变原因的评估。

Evaluation of anorexia as the cause of altered protein synthesis in skeletal muscles from nongrowing mice with sarcoma.

作者信息

Lundholm K, Karlberg I, Ekman L, Edström S, Scherstén T

出版信息

Cancer Res. 1981 May;41(5):1989-96.

PMID:6163532
Abstract

The importance of decreased food intake as the mechanism behind altered protein metabolism in skeletal muscle in cancer was evaluated. A methylcholanthrene-induced sarcoma (MCG 101) transplanted in weight-stable and nongrowing mice (C57BL/6J) was used as the tumor-animal model. Three study groups with appropriate control groups were used: sarcoma-bearing mice; pair-fed mice; and starved mice. The synthesis of myofibrillar and sarcoplasmic proteins was decreased in sarcoma-bearing mice. This was correlated to decreased content of RNA in the muscles and caused a net loss of muscle tissue was measured by dry weight of skeletal muscles. The incorporation rate of amino acids into myofibrillar and sarcoplasmic proteins was decreased to the same extent in the pair-fed mice as that in the sarcoma-bearing mice. This probably reflected decreased protein synthesis, since the radioactivity (dpm/mg) did not differ significantly in the crude transfer RNA fraction between the groups. Separation of soluble proteins from muscle tissue by means of ion-exchange chromatography showed that the pattern of decreased protein synthesis was not tumor specific when compared to muscle affected by starvation. The decrease in protein synthesis was more or less selective, since the synthesis of basic proteins was considerably decreased and was influenced more than were neutral and acidic proteins in both cancer and starvation. Anorexia of a tumor-bearing host is a sufficient trigger to induce decreased protein synthesis in skeletal muscles, but other factors may also be of quantitative importance.

摘要

评估了食物摄入量减少作为癌症患者骨骼肌蛋白质代谢改变背后机制的重要性。将甲基胆蒽诱导的肉瘤(MCG 101)移植到体重稳定且未生长的小鼠(C57BL/6J)中,作为肿瘤动物模型。使用了三个研究组及相应的对照组:荷瘤小鼠;配对喂养小鼠;饥饿小鼠。荷瘤小鼠肌原纤维蛋白和肌浆蛋白的合成减少。这与肌肉中RNA含量的降低相关,并导致通过骨骼肌干重测量的肌肉组织净损失。在配对喂养小鼠中,氨基酸掺入肌原纤维蛋白和肌浆蛋白的速率降低程度与荷瘤小鼠相同。这可能反映了蛋白质合成的减少,因为各组之间粗转移RNA组分中的放射性(dpm/mg)没有显著差异。通过离子交换色谱法从肌肉组织中分离可溶性蛋白质表明,与受饥饿影响的肌肉相比,蛋白质合成减少的模式并非肿瘤特异性。蛋白质合成的减少或多或少具有选择性,因为碱性蛋白质的合成显著减少,并且在癌症和饥饿状态下,其受到的影响均大于中性和酸性蛋白质。荷瘤宿主的厌食是诱导骨骼肌蛋白质合成减少的充分诱因,但其他因素在数量上可能也很重要。

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