Amylin is a 37-amino acid P-cell hormone, which is co-located and co-secreted with insulin in response to nutrient intake. In persons without diabetes, the pattern of amylin and insulin secretion throughout the day is similar: low fasting concentrations that rapidly increase following meals (Fig. 1) (3-6). Preclinical experiments in rodents have demonstrated that amylin exerts its effects as a neuroendocrine hormone, activating specific amylin receptors in the brain (7,8). Via this central binding, amylin stimulates three key actions that together help control the rate of glucose appearance into the circulation during the postprandial period. Amylin suppresses postprandial glucagon secretion (9-12), modulates the rate of gastric emptying (13,14), and attenuates feeding behavior (15,16). Since one of the primary actions of insulin in the postprandial period is promotion of glucose disappearance (into peripheral tissues), amylin, with its effects on glucose appearance, can be considered a partner or complementary hormone to insulin, with both hormones contributing to the maintenance of normal postprandial glucose concentrations (Fig. 2). Given the characteristics of P-cell dysfunction in diabetes, there is an absolute deficiency of insulin and amylin in patients with type 1 diabetes and a progressive decline of insulin and amylin secretory capacity in patients with type 2 diabetes (Fig. 3) (3,5,17).
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