This article summarizes the key literature describing the effects of the pancreatic beta-cell hormone amylin on eating. One of the first described and best investigated effects of amylin on eating is its physiological effect to control meal size by inducing satiation. This effect is very rapid, short-lasting and probably directly reflects the meal-induced increase in circulating amylin levels. Evidence provided by many groups suggests that the effect of amylin on eating is directly mediated by humoral action in the central nervous system rather than by peripheral receptors. It is also clear that the caudal hindbrain, in particular the area postrema, is a key brain region mediating amylin effects, but amylin may also act at different sites in the brain. The latter is particularly true for the effect of amylin to reduce food reward. Hence, amylin not only reduces caloric intake as such but may specifically reduce high fat intake, at least in certain experimental conditions; in people, amylin receptor agonists have been shown to reduce the number of binge eating episodes. In recent years, long-lasting amylin receptor agonists have been developed. Alone or in combination with other gut hormone receptor agonists (in particular the agonist of glucagon-like peptide-1 [GLP-1] receptor, semaglutide), these molecules turned out to be highly promising therapeutic agents for the treatment of obesity.