The neural circuits that control food intake and energy administration are not fully characterized. Leptin from adipocytes, ghrelin from the stomach, glucagon-like peptide 1 (Glp-1) as well as insulin address neurons in a primary energy homeostatic center: the hypothalamic arcuate nucleus with the neuropeptides Y (NPY, orexigenic peptide) and melanocortin neurons, which produce the anorexigenic peptide alpha-melanocyte stimulating hormone (alpha-MSH). An involvement of the histaminergic system in regulation of feeding behaviour was shown in several studies. It has been proposed that anorectic peptidergic pathways (leptin, GLP-1, Gotoh et al. 2005) converge on histaminergic neurons of the tuberomamillary nucleus (TMN), which project all over the brain and regulate arousal and energy expenditure. A direct action of feeding-related peptides was investigated. The firing rate of histaminergic neurons was recorded in rat brain slices in cell-attached mode and in cultured posterior hypothalamic neurons with microelectrode array (MEA) techniques. Insulin and Glp-1 increased the firing rate of TMN neurons, but there was no direct action for leptin, alpha-MSH, ghrelin and NPY. Thus, the selected satiety peptides directly recruit the histaminergic system, while others act indirectly to reduce feeding behaviour. This regulation is deeply disturbed in hepatic encephalopathy, where enhanced histamine production is accompanied by increased food intake (Fogel et al 2008).