Neuroendocrine hormone amylin in diabetes

Abstract

The neuroendocrine hormone amylin, also known as islet amyloid polypeptide, is co-localized, co-packaged and co-secreted with insulin from adult pancreatic islet β cells to maintain glucose homeostasis. Specifically, amylin reduces secretion of nutrient-stimulated glucagon, regulates blood pressure with an effect on renin-angiotensin system, and delays gastric emptying. The physiological actions of human amylin attribute to the conformational α-helix monomers whereas the misfolding instable oligomers may be detrimental to the islet β cells and further transform to β-sheet fibrils as amyloid deposits. No direct evidence proves that the amylin fibrils in amyloid deposits cause diabetes. Here we also have performed a systematic review of human amylin gene changes and reported the S20G mutation is minor in the development of diabetes. In addition to the metabolic effects, human amylin may modulate autoimmunity and innate inflammation through regulatory T cells to impact on both human type 1 and type 2 diabetes.

Keywords: Amylin; Neuroendocrine hormone; Diabetes

Core tip: This is a systematic review to describe amylin as a neuroendocrine hormone. Besides the glucose homeostasis and cytotoxicity of amylin, we tried to perform that the S20G mutation of human amylin is also minor in the pathogenesis of diabetes. In addition to the metabolic effects, human amylin may have impact on autoimmunity, implicating a potential as the immunosuppressor to improve autoimmunity conditions in the future therapy of diabetes, allergic diseases and immune rejection.