Pancreatic Islet Amyloid and Diabetes
Protein Misfolding, Aggregation, and Conformational DiseasesProtein Reviews(2007)
Abstract
Deposition of amyloid in pancreatic islets is a feature of type 2 diabetes in man but the causal factors are unknown. Progressive
amyloidosis results in loss of insulin-producing cells and increased severity of disease. The fibril component is a 37-amino-acid
peptide, islet amyloid polypeptide (IAPP; amylin), which is a normal cellular peptide, cosecreted with insulin; the species-specific
amino-acid sequence of IAPP is unaltered in diabetes. Peptide refolding in islet perivascular spaces to form β-sheets could
be related to production of fragments of the precursor peptide, proIAPP. Islet amyloidosis is not a causal factor for hyperglycemia
in man but contributes to onset of diabetes in non-human primates and transgenic rodent models. Because islet amyloidosis
cannot be detected in vivo, clinical development of inhibitors is likely to be difficult.
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