Obesity develops despite a complex and seemingly well orchestrated network that controls eating, energy expenditure and ultimately body weight; many of the involved signals are derived from the gastrointestinal tract. It is assumed that this network as an entity aims at maintaining body weight and body adiposity at a relatively constant level, but the control mechanisms seem to fail at least if an individual is chronically exposed to an oversupply of food. This article summarizes recent findings about the role of amylin in the control of eating in lean and obese rodents. The article gives some short background information about the well investigated adiposity and satiating signals leptin and cholecystokinin, respectively; this will provide the framework to discuss aspects of amylin physiology and pathophysiology in the control of eating in leanness and obesity. This discussion also involves the mechanisms mediating amylin's eating inhibitory effect in the area postrema and the interactions between amylin and leptin. Further, we discuss the effect of high fat diets on amylin release and amylin action in lean and obese rats. The last part of this article raises the question whether amylin interacts with the reward system in the forebrain.