Ventromedial hypothalamic and paraventricular nucleus lesions damage a common system to produce hyperphagia.

We investigated the anatomical basis of paraventricular (PVN) and ventromedial (VMH) hypothalamic hyperphagia. Asymmetrical electrolytic lesions, damaging the VMH and PVN contralaterally, produced significant hyperphagia and weight gains (mean = 257.2 g) almost three times those of controls (89.8 g) during 56 postsurgical days. Weight gain in these rats was not significantly different from that in rats with bilateral lesions of the VMH (277.2 g) or PVN (188.2 g). Combined bilateral destruction of the PVN and VMH produced weight gain (272.8 g) almost identical to that seen after bilateral VMH lesions alone. The lack of additivity of these combined lesions and the effectiveness of the asymmetrical lesions are consistent with the hypothesis that lesions of either of these two regions damage a longitudinally running system to produce elevated food intake and body weight. Cell bodies of this system may lie within the PVN and send efferent projections through the VMH. Hyperinsulinemia developed only in rats with bilateral damage in the VMH. Thus, hypothalamic hyperphagia and hyperinsulinemia appear to be dissociable, reflecting damage to separate neural systems.