Eating behavior is a complex phenomenon, resulting from the interaction in the hypothalamus and other brain regions, of many factors, including olfactory, visual, emotional and higher cognitive inputs, as well as several nutritional signals coming from the periphery. These signals modulate the expression of neurotransmitters and neuropeptides with orexigenic and anorexigenic activity. Observations performed more than 5 decades ago with brain lesioning and stimulation experiments led to the proposal of the dual centre hypothesis in the central control of energy balance. On the basis of these studies the "satiety centre" was located in the ventromedial hypothalamic nucleus, since lesions of this region caused overfeeding, while its electrical stimulation suppressed eating. On the contrary, lesioning or stimulation of the lateral hypothalamus elicited the opposite set of responses, thus leading to the conclusion that this area represented the "feeding centre". The subsequent expansion of our knowledge of specific neuronal subpopulations involved in energy homeostasis has replaced the notion of specific "centres" controlling energy balance with that of discrete neuronal pathways fully integrated in a more complex neuronal network. This review will focus on the central and peripheral factors thought to be involved in the neuroendocrine control of feeding behavior.