Abstract
Obesity is a disease that is both costly and prevalent, and although the development and use of glucagon-like peptide-1 receptor agonists has dramatically altered the landscape of obesity treatment, there remains a need to identify alternate approaches to reduce body weight. Amylin, a pancreatic hormone, has been viewed as a favorable candidate for novel obesity pharmacotherapies due to its ability to suppress feeding and body weight through its actions in the brain. Although research initially focused on hindbrain sites of action for amylin, more recent work has identified other central nuclei at which amylin influences food intake and food reward. This review discusses the growing body of literature suggesting that amylin signaling in mesolimbic structures of the brain influences food intake and reward processing. These effects are observed for palatable food as well as other reinforcing stimuli such as drugs of abuse. This is an important area of research as the broad effects of amylin-based pharmacotherapies should be considered when developing new obesity medications.