Activation of UCPs gene expression in skeletal muscle can be independent on both circulating fatty acids and food intake involvement of ROS in a model of mouse cancer cachexia
Activation of UCPs gene expression in skeletal muscle can be independent on both circulating fatty acids and food intake involvement of ROS in a model of mouse cancer cachexia
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DOI：
10.1016/j.febslet.2004.12.050
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发表时间：
2005-01-31
期刊：
影响因子：
3.5
通讯作者：
López-Soriano, FJ
中科院分区：
文献类型：
--
作者：
Busquets, S;Almendro, V;López-Soriano, FJ
将快速生长的肿瘤(Lewis肺癌)移植到小鼠身上，导致了一种明显的恶病质状态，特征是严重的肌肉萎缩。伴随而来的是骨骼肌和心脏中UCP2和UCP3基因表达的显著增加。有趣的是，这种基因表达的增加与循环脂肪酸的增加或食物摄入量的减少并不相关，正如之前在其他病理生理状态中所报道的那样。这些结果质疑了高脂血症是在不同病理生理条件下控制UCP基因表达的唯一因素的观点。此外，目前的工作表明，UCPs可能参与了一个反调节机制，以降低ROS的产量。(C)2005年欧洲生化学会联合会。爱思唯尔出版，版权所有。
Implantation of a fast growing tumour to mice (Lewis lung carcinoma) resulted in a clear cachectic state characterized by a profound muscle wasting. This was accompanied by a significant increase in both UCP2 and UCP3 gene expression in skeletal muscle and heart. Interestingly, this increase in gene expression was not linked to a rise in circulating fatty acids or in a decrease in food intake, as previously reported in other pathophysiological states. These results question the concept that hyperlipaemia is the only factor controlling UCP gene expression in different pathophysiological conditions. In addition, the present work suggests that UCPs might participate in a counter-regulatory mechanism to lower the production of ROS. (C) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.