Lesions of the ventromedial hypothalamus (VMH) result in an obesity syndrome with several metabolic and behavioral manifestations. It has also been reported that damage to the paraventricular hypothalamus (PVH) leads to changes characteristic of obesity. However, little is known about the consequence of PVH lesions, especially in contrast to the extensive documentation of VMH lesion-induced effects. To assess the basic features of the two hypothalamic obesity syndromes, rats underwent VMH, PVH, or sham lesions and, for 15 weeks, were maintained ad lib on a series of test diets. Both lesions groups were hyperphagic and showed similar weight gains. Although both lesion groups became obese (measured by % carcass fat), VMH rats were fatter than PVH animals. Similarly, only VMH rats were hyperinsulinemic. Further tests were conducted in PVH and VMH rats restricted to control body weights. VMH, but not PVH, rats developed a persisting elevation in basal gastric acid secretion. As well, only VMH, and not PVH, animals developed an obesity when restricted to normal weights. These data indicate similarities in PVH and VMH rats maintained ad lib but experiments on restricted animals reveal fundamental differences in the two obesities and point to different etiologies.