Metabolic stress, IAPP and islet amyloid

Joel Montané Mogas, A. Klimek-Abercrombie, K. J. Potter, C. Westwell-Roper, C. Bruce Verchere

Producció científica: Article en revista indexadaArticleAvaluat per experts

76 Cites (Scopus)


Amyloid forms within pancreatic islets in type 2 diabetes from aggregates of the β-cell peptide islet amyloid polypeptide (IAPP). These aggregates are toxic to β-cells, inducing β-cell death and dysfunction, as well as inciting islet inflammation. The β-cell is subject to a number of other stressors, including insulin resistance and hyperglycaemia, that may contribute to amyloid formation by increasing IAPP production by the β-cell. β-Cell dysfunction, evident as impaired glucose-stimulated insulin secretion and defective prohormone processing and exacerbated by metabolic stress, is also a likely prerequisite for islet amyloid formation to occur in type 2 diabetes. Islet transplants in patients with type 1 diabetes face similar stressors, and are subject to rapid amyloid formation and impaired proinsulin processing associated with progressive loss of β-cell function and mass. Declining β-cell mass is predicted to increase metabolic demand on remaining β-cells, promoting a feed-forward cycle of β-cell decline.
Idioma originalAnglès
Pàgines (de-a)68-77
Nombre de pàgines10
RevistaDiabetes, Obesity and Metabolism
NúmeroSuppl. 3
Estat de la publicacióPublicada - d’oct. 2012


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