Female rats with electrolytic lesions of the ventromedial hypothalamus (VMH) were pair fed with controls in a new paradigm in which food was delivered in normal temporal patterns, i.e., those of nonlesioned rats bar pressing for food. Lesions were produced after 6 days of adaptation to this regimen, and the experiment continued for 30 days postlesion. When they were killed, VMH rats contained substantially more carcass lipid than controls (20.4 vs. 12.4%) and were hyperinsulinemic (67.2 vs. 27.6 microunits/ml). Because these elevations developed in the absence of even minor disturbances in feeding patterns, these results support the view that VMH damage confers an essential metabolic bias favoring obesity. Separate VMH groups pair fed exclusively by either oral or intragastric routes exhibited virtually identical exaggerations in fat accumulation (18.4 and 17.7 g above controls, respectively) and plasma insulin (69.2 and 65.4 microunits/ml, respectively). Thus, contrary to a prediction of one form of Powley's (Powley, T. L. Psychol. Rev. 84:89–126, 1977) cephalic phase hypothesis, oropharyngeal stimulation and, hence, the cephalic responses of digestion are not critical for the metabolic disturbances that follow VMH damage.