Morrison S D
Cancer Res. 1976 Jan;36(1):228-33.
Daily food intake and corresponding feeding activity (measured as duration) and feeding efficiency (amount of food ingested per unit of feeding activity) were measured both in normal Sprague-Dawley and Buffalo rats and during growth of Walker 256 and 4M mammary carcinomas in Sprague-Dawley rats and of Morris 5123 hepatoma in Buffalo rats. Estimates of meal size and frequency were also obtained. Growth of the carcinomas produced a decline in feeding activity accompanied, early in tumor growth, by a compensatory increase in feeding efficiency with no resultant effect on food intake. This compensated decline in feeding activity was due to reduction in average meal duration. Later, meal frequency was also reduced, with further reduction in feeding activity and reduction in food intake. There was little change in average meal size. The hepatoma produced a different detailed pattern of effect on feeding behavior. These effects are not nonspecific reactions to foreign tissue. The effects imply behavioral compensation for the breakdown of a rapidly responding physiological control of food intake and can be interpreted in terms of successive impairment of feeding control mechanisms that have different response rates and different behavioral modes.
在正常的斯普拉格-道利大鼠和布法罗大鼠中，以及在斯普拉格-道利大鼠的沃克256和4M乳腺癌以及布法罗大鼠的莫里斯5123肝癌生长期间，测量了每日食物摄入量以及相应的进食活动（以持续时间衡量）和进食效率（每单位进食活动摄入的食物量）。还获得了餐量和进食频率的估计值。癌症的生长导致进食活动减少，在肿瘤生长早期，进食效率会相应增加以进行补偿，而食物摄入量没有变化。这种进食活动的补偿性下降是由于平均进餐持续时间缩短所致。后来，进餐频率也降低了，进食活动进一步减少，食物摄入量也减少。平均餐量变化不大。肝癌对进食行为产生了不同的具体影响模式。这些影响并非对外来组织的非特异性反应。这些影响意味着对快速反应的食物摄入生理控制机制的破坏进行行为补偿，并且可以根据具有不同反应速率和不同行为模式的进食控制机制的相继受损来解释。
