Amylin is a fibrillogenic protein co-secreted with insulin from pancreatic beta cells. Amylin has been shown to function in metabolism through its influence on glucose homeostasis. It has also been proposed to have an impact on amyloid beta, a major component of the amyloid plaques found in Alzheimer’s disease. Alzheimer’s disease brains have been shown to have amyloid plaque formation and decreased expression of Uncoupling Protein 2 (UCP2). Knowing that UCP2 is expressed in pancreatic beta cells and has been shown to have diminished levels in Alzheimer’s disease brains the focus of this study was to examine the influence of UCP2 on the presence and expression of amylin in both RIN-5F cells (a pancreatic beta cell line) and SH-SY5Y cells (a neuroblastoma cell line). Immunocytochemistry experiments and ELISA assays were conducted with Genipin, a molecule that knockdowns the presence of UCP2, to examine both the presence of amylin and the activity level of amylin, respectively.