Abstract

Prior to hypothalamic surgery 1 group of male rats was placed on a partial starvation regimen to lower their body weight. A second group was fed ad libitum. Just before surgery the 2 groups were divided into 2 sub groups. Bilateral electrolytic lesions were then placed in the dorsomedial hypothalamic nucleus in some of the partially starved and some of the ad libitum fed rats. The remaining animals were sham operated. After surgery all groups were fed ad libitum. Following hypothalamic operation the group that before surgery had been fed ad libitum showed the previously reported postoperative hypophagia and reduced body weight. On the other hand, the rats that were partially starved prior to placement of the lesion, ate significantly more than ad libitum fed lesioned animals during the first 9 days after surgery. The body weights of the partially starved, lesioned rats increased steadily from the day of the operation while lesioned rats fed ad libitum showed an initial delay of ponderal growth. The data suggest that the transient postoperative increase in food intake of the partially starved, lesioned rats is an active process to bring the body weight of these animals up to a new but lowered ‘body weight set point’ initiated by the hypothalamic destruction. Since previous studies had shown that rats with a lesion in the dorsomedial nucleus have a normal body composition, it is suggested that the lesions change the animals' ‘body weight set point’ and not the ‘body fat set point’, as has been suggested after ventromedial and lateral hypothalamic lesions.

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