Commentary

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

Volume 3, Issue 1   January/February 2011
Pages 38 - 39
http://dx.doi.org/10.4161/isl.3.1.14258
Authors: Kerry M. Loomes

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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 mass1,2 and the occurrence of insoluble amyloid deposits within the islets of Langerhans.1,3 These amyloid deposits comprise predominantly of fibrillar aggregates of the 37-amino acid human amylin (hA) monomer,4 also known as islet amyloid polypeptide (IAPP),5 which is co-secreted with insulin from pancreatic islet β-cells via the regulated secretory pathway.6,7 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).

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