The rate of wt. gain, changes in food consumption, the duration of the various phases of exptly. produced obesity and the loci of obesity -producing lesions were detd. in a series of albino rats. Neither limitation of the daily food intake to that of the pre-operative period nor pair-feeding with normal controls prevented development of a degree of obesity. This advantage conferred by the lesion is slight, however, and animals with lesions were never able to outgain normal animals which were forced by limitation of food intake to compensate metabolically in order to maintain body wt. Prevention of temporary engorgement with food by spaced feedings did not prevent obesity but potentially obese animals were not able to outgain normal rats which had been forced to compensate metabolically in order to maintain their body wts. under conditions imposed by feeding regimes. Hyper-phagia due to hypothalamic injury was not abolished by long continued limitation of food. Periods of starvation were followed by an augmentation of appetite and development of a greater degree of obesity than had been attained before fasting. The major cause of this experimentally produced obesity was the breakdown of the balance between food intake and energy utilization. Inappropriate augmentation of the appetite was presumably accompanied by a less significant decrease in caloric requirement.