Control of food intake in experimental tumor growth.
The cachectic depletion of cancer is invariably an immediate consequence of progressive deficit of food intake below metabolic cost. The deficit of food intake arises from successive impairment of individual feeding controls. The impairment of some feeding controls well before there is overt hypophagia or cachexia indicates that overt cachexia is preceded by a silent or compensated cachectic process, and behavioral compensation for deteriorating feeding controls can be demonstrated. The hypothalamic components of control of food intake are not affected. In some instances, severe asthenic reduction in motor activity further disables capacity to feed since feeding is a motor activity and motor capability is a necessary condition for feeding. The variability in timing and severity of cachectic decay among different tumors and individuals is a function of the timing and sequencing of breakdown of individual controls, capacity for compensation, and impairment of motor capability, and the extent to which all possible controls are functionally expressed in the normal individual.
D000818:Animals; D001247:Asthenia / Q000150:complications; D002100:Cachexia / Q000209:etiology; D001068:Feeding and Eating Disorders / Q000209:etiology*; D006801:Humans; D009374:Neoplasms, Experimental / Q000150:complications*; D051381:Rats; D011919:Rats, Inbred Strains