Tisdale M J, Beck S A
CRC Experimental Chemotherapy Group, Aston University, Birmingham, UK.
Int J Pancreatol. 1990 Aug-Nov;7(1-3):141-50. doi: 10.1007/BF02924231.
Cancer cachexia has been listed as a major cause of death in cancer patients. In order to investigate the metabolic effects of the tumor on the host, we have evaluated an experimental model of cancer cachexia in the mouse (MAC16 colon adenocarcinoma), in which weight loss can reach 30-40% of initial weight with a tumor burden of only 2.5%, without a reduction in the intake of either food or water. The weight loss appears not to arise from tumor necrosis factor production, which is associated with a marked reduction in both food and water intake, but may be a result of catabolic factors produced by the tumor and present in the circulation. Both insulin and 3-hydroxybutyrate are effective inhibitors of the tumor catabolic factors in vitro and protect, to some extent, weight loss in vivo. However, whereas 3-hydroxybutyrate was associated with a reduction in tumor weight, insulin caused an enhancement, suggesting that the former may be more appropriate than the latter in the clinical treatment of cancer cachexia.
癌症恶病质已被列为癌症患者的主要死因之一。为了研究肿瘤对宿主的代谢影响,我们评估了小鼠癌症恶病质的实验模型(MAC16结肠腺癌),在该模型中,肿瘤负荷仅为2.5%时,体重减轻可达初始体重的30 - 40%,而食物和水的摄入量均未减少。体重减轻似乎并非由肿瘤坏死因子产生所致,肿瘤坏死因子会导致食物和水的摄入量显著减少,体重减轻可能是肿瘤产生并存在于循环系统中的分解代谢因子所致。胰岛素和3 - 羟基丁酸在体外都是肿瘤分解代谢因子的有效抑制剂,在一定程度上可防止体内体重减轻。然而,3 - 羟基丁酸与肿瘤重量减轻有关,而胰岛素则导致肿瘤重量增加,这表明在癌症恶病质的临床治疗中,前者可能比后者更合适。