Amylin is a 37-amino acid peptide hormone that is co-secreted with insulin by pancreatic B cells in response to food intake. Exogenous amylin potently and dose-dependently reduces feeding in rats and mice, with both central and peripheral sites being effective. Although amylin has been characterized as a satiety signal that regulates short-term food intake (i.e., meal size), recent data indicate that amylin may have long term effects on food intake and body weight. In fact, amylin shares many properties with the established adiposity signals, leptin and insulin. Like leptin and insulin, amylin is not synthesized within the brain, but is rapidly and efficiently transported across the blood-brain barrier (BBB) to a variety of discrete brain regions, including the hypothalamus, where populations of amylin binding sites are found. Further, amylin secretion and plasma levels are correlated with the degree of body adiposity, as is the case for leptin and insulin. In the following brief review, a summary of the findings from recent reports is presented supporting the hypothesis that amylin's role in the control of food intake is not limited to that of purely a satiety signal that brings individual bouts of ingestion to an end, but also serves as an adiposity signal acting within the brain to regulate long-term energy homeostasis.