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Amylin physiologically controls satiation, slows gastric emptying and limits postprandial glucagon release, while its actions also link homeostatic eating controls with reward driven behaviours via defined central nervous system pathways. Further, at least under certain conditions, aggregating amylin exerts a strong pathophysiological impact on the destruction of pancreatic beta\u2010cells in Type 2 diabetes mellitus (T2D), providing a plausible explanation for why a T2D\u2010like disease entity is only observed in a few mammalian species. 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