The control of eating is part of the homeostatic regulation of energy stores, metabolites and essential nutrients. Meal initiation and termination result from signals originating in the oral cavity (orosensory stimuli), in the gastrointestinal tract (stomach distension, nutrients, osmolality), and from the metabolization of absorbed nutrients. In addition, signals reflecting the amount of fat stored in the body supposedly modulate the central nervous system (CNS) integration of the meal-related neural (afferent nerve activity) and humoral (e.g. gut peptides) signals, which ultimately shapes the behavioural (eating) and autonomic (metabolism) response. Gut peptides released from enteroendocrine cells in response to luminal nutrient stimulation can influence eating through an endocrine effect or through a paracrine action on afferent nerves in the gut. Some gut peptides also have potent insulinotropic and gluco-regulatory effects, making them attractive candidates for the pharmacotherapy of obesity and type II-diabetes. Besides stimulating gut peptide release, eating causes an immune reaction in the gut. Thus, fat intake can trigger inflammatory reactions that may change the response to satiating gut peptides. Systemic immune challenges inhibit eating through pro-inflammatory cytokines that can act on CNS neurons through vagal afferent signalling, by stimulating the release of neuromodulators from blood brain barrier (BBB) epithelial cells, or after active transport across the BBB. In any case, the signalling pathways converge on the same CNS circuits that control normal eating. Whether the immune reaction induced by a meal is strong enough to inhibit eating is unknown. Here I review the various gut peptide and inflammation-related mechanisms that affect eating and their potential interactions.