Biologic and behavioral studies on the control of appetite and satiety have shifted their focus markedly during the past two decades. A former preoccupation with the “dual-center” model, whereby food intake was controlled by a lateral hypothalamic feeding center and a medial hypothalamic satiety center, was based largely on investigations in which the putative centers were destroyed by stereotaxic electrolytic lesions. lq2 This familiar idea has now been discarded by most investigators in light of subsequent observations that have caused a reinterpretation of the initial results. Specifically, the prolonged period of aphagia seen after lateral hypothalamic lesions appears to result from destruction of dopaminergic neurons ascending through the lateral hypothalamic area and reflects a decrease in cerebral arousal that precludes all voluntary behaviors, not just feeding. 3s4 Moreover, the syndrome of hyperphagia and obesity after medial hypothalamic lesions seems to derive primarily from hyperinsulinism associated with a decrease in sympathetic tone, as a result of which ingested calories are rapidly and preferentially stored via lipogenesis rather than utilized gradually for ongoing metabolic demands5V6