Glucose homeostasis is accomplished through intricate, and arguably, elegant interactions among several organs and hormones. Historically, glucose homeostasis has been viewed somewhat narrowly--insulin from pancreatic beta cells regulated glucose disposal, while glucagon from pancreatic alpha [corrected] cells regulated glucose appearance during fasting states. But more recent characterization and understanding of the role of incretin hormones from the gut--notably, glucagon-like peptide 1 and gastric inhibitory polypeptide--and amylin from pancreatic beta cells has led to a more complete model of glucose homeostasis. Furthermore, availability of pharmacologic agents to replace, mimic, or enhance the actions of these hormones allows application of this more complete model of glucose homeostasis to the treatment of type 1 and type 2 diabetes. This article provides an overview of the role of the pancreatic hormone amylin in glucose homeostasis and of Pramlintide, a analogue of native amylin, recently approved as adjunct therapy to insulin in people with type 1 and type 2 diabetes.