Survival of an islet β-cell in type-2 diabetes: curbing the effects of amyloid cytotoxicity.
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).
School of Biological Sciences, Institute for Innovation in Biotechnology, and Maurice Wilkins Centre for Molecular Biodiscovery, University of Auckland, Auckland, New Zealand. k.loomes@aukland.ac.nz
Kerry M
KM
Loomes
D000682:Amyloid / Q000633:toxicity*; D000818:Animals; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D019610:Cytoprotection / Q000187:drug effects / Q000502:physiology; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology*; D006801:Humans; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000502:physiology*; D007515:Islets of Langerhans / Q000187:drug effects / Q000502:physiology*
D000682:Amyloid