Morrison S D
Cancer Res. 1982 Sep;42(9):3642-7.
The Walker 256 carcinosarcoma growing in Sprague-Dawley rats and the Morris 5123 hepatoma growing in Buffalo rats both produce cachexia but have widely differing patterns of host metabolism and tumor growth. Both organisms respond to exogenous insulin with increased food intake and rate of weight gain of host. The insulin treatment response of food intake was 1.5 to 2 times and of body weight gain was 2 to 3 times that of tumor-free controls. Insulin does not accelerate tumor growth. On withdrawal of insulin, the reactive hypophagia seen in tumor-free rats does not occur in tumor bearers, and the host weight does not return to the expected untreated value as it does in tumor-free rats. Most of the weight gained during insulin treatment of tumor bearers above that gained by tumor-free rats is retained after withdrawal of insulin. A computer model based on the inference from these results, that the tumor-bearing host is blind to body weight error, indicates that this abnormality of feeding control could account for only about one-third of the observed depression of host weight and food intake.
生长于斯普拉格-道利大鼠体内的沃克256癌肉瘤和生长于布法罗大鼠体内的莫里斯5123肝癌均会导致恶病质，但宿主代谢模式和肿瘤生长方式却大不相同。两种生物对外源性胰岛素的反应均为宿主食物摄入量增加和体重增加速率加快。胰岛素治疗对食物摄入量的反应是无肿瘤对照组的1.5至2倍，对体重增加的反应是无肿瘤对照组的2至3倍。胰岛素不会加速肿瘤生长。停用胰岛素后，无肿瘤大鼠出现的反应性摄食减少在荷瘤大鼠中并未出现，且宿主体重不会像无肿瘤大鼠那样恢复到预期的未治疗值。荷瘤大鼠在胰岛素治疗期间比无肿瘤大鼠多增加的大部分体重在停用胰岛素后得以保留。基于这些结果推断得出的一个计算机模型表明，荷瘤宿主对体重误差不敏感，该模型指出这种摄食控制异常仅能解释所观察到的宿主体重和食物摄入量下降的约三分之一。
