354 



p. TEITELBAUM AND A. N. EPSTEIN 



provide the additional motivation necessary for regulation. In these 

 animals, the shghtest change in the taste of food or water may mean the 

 difference between Hfe or death. 



There are two kinds of disturbances in feeding that result from hypotha- 

 lamic damage. Overeating results from lesions in the vicinity of the ven- 

 tromedial nuclei. Starvation occurs after damage to the lateral hypo- 

 thalamic areas. Let us first consider hypothalamic hyperphagia. There 

 appears to be no metabolic disturbance in animals with ventromedial 

 hypothalamic lesions — they get fat because they eat too much (Brobeck, 

 Tepperman and Long, 1943). There are two phases in hypothalamic 

 hyperphagia : an initial dynamic phase, immediately following the opera- 

 tion, in which the animal eats two to three times as much as normal, and 

 gains weight rapidly. Then after the animal has become obese, a static 

 phase ensues, in which the weight levels off at a high plateau and the 

 animal's food intake drops back to only slightly more than normal. How 

 well do such animals regulate their food intake in the face of changes in the 

 quality of the diet? Figure 6 shows the results of an experiment in which 



< 

 en 

 o 



< 



Fig. 6. 



5 15 25 50 75 5 15 25 



% RUFFEX ADULTERATION 



Food intake of normal and hyperphagic animals when oifered a diet 

 mixed with non-nutritive cellulose. (From Teitelbaum, 1955.) 



the diet was adulterated with non-nutritive bulk (Teitelbaum, 1955). 

 As described previously, normal animals regulate their intake when almost 

 half the diet is non-nutritive cellulose, and eat appreciable amounts even 



