Survival of an islet β-cell in type-2 diabetes: curbing the effects of amyloid cytotoxicity

Islets. Jan-Feb 2011;3(1):38-9. doi: 10.4161/isl.3.1.14258. Epub 2011 Jan 1.

Abstract

Type 2 diabetes mellitus is a chronic hyperglycaemic disorder caused by defective action and secretion of insulin. It is characterized by a progressive decline in pancreatic β-cell function and mass and the occurrence of insoluble amyloid deposits within the islets of Langerhans. These amyloid deposits comprise predominantly of fibrillar aggregates of the 37-amino acid human amylin (hA) monomer, also known as islet amyloid polypeptide (IAPP), which is co-secreted with insulin from pancreatic islet β-cells via the regulated secretory pathway. hA has a propensity to aggregate in vitro into fibrillar structures through the self-association of monomers that is largely mediated by an amyloidogenic region spanning amino acids 20-29 (reviewed in ref. 8).

Publication types

  • Review

MeSH terms

  • Amyloid / toxicity*
  • Animals
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Cell Survival / physiology
  • Cytoprotection / drug effects
  • Cytoprotection / physiology
  • Diabetes Mellitus, Type 2 / physiopathology*
  • Humans
  • Insulin-Secreting Cells / drug effects
  • Insulin-Secreting Cells / physiology*
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / physiology*

Substances

  • Amyloid