The role of amylin in the physiology of glycemic control

Abstract

Amylin is a 37-amino acid peptide hormone, discovered in 1987, which is co-located and co-secreted with insulin by the pancreatic beta-cells in response to nutrient stimuli. Like insulin, there is a deficiency of amylin in people with type 1 diabetes, while the changes in plasma amylin concentrations in people with impaired glucose tolerance and type 2 diabetes parallel those of insulin. It is well established that insulin regulates glycemic control by promoting glucose disposal. This paper reviews evidence from studies in animals and people with diabetes that amylin regulates the inflow of glucose to the circulation by delaying nutrient delivery and, thus, the appearance of meal-derived glucose, and also suppresses glucagon secretion in the postprandial period. It is suggested, therefore, that the actions of amylin complement those of insulin, and that the problems of glycemic control which continue to exist in people with diabetes, despite insulin replacement therapy, may be attributable to a deficiency in amylin. Preclinical and clinical studies with pramlintide, a synthetic analogue of human amylin, are also included in this brief review.