Variability of body fat in hyperphagic rats.

Although hypothalamic hyperphagia was described and named 25 years ago,: the nature of this phenomenon is still not clear. Presumably it is brought about by some deficiency in the systems controlling food intake. What this deficiency might be was explicitly considered by Kennedy' in the paper where he suggested that the body regulates its fat content. He had confirmed the observation of Brobeck, Tepperman, and Long' that one of the characteristics of this hyperphagia is that it tends to disappear as the animal becomes obese. Kennedy decided that the obesity more or less directly antagonizes the hyperphagia, and wrote as follows: "The only invariable index of the loss of hypothalamic function is the level of obesity which develops. .. Once the level of fatness is determined, it is actively maintained. .. The only disturbance of appetite which ever does develop, in fact, is the transient increase incidental to getting fat."' His view of these phenomena has been accepted into the literature as the "lipostatic" hypothesis of control of food intake. According to this hypothesis , the hypothalamus adjusts food intake so as to regulate the size of fat depots. After ventromedial lesions the food intake is increased because the control system is given a new set point that requires a greater amount of fat in the body. When this greater amount has been acquired, the system functions to maintain energy balance as before. In subscribing to this hypothesis , Teitelbaum' has written, ".. . then one might say that the hyper-phagic rat overeats to get fat. Once it is fat, it no longer overeats" (p. 49). Some animals with hypothalamic lesions become more obese than other animals, presumably because the effectiveness of ventromedial lesions varies from one animal to another; in any given animal, however, the effective