Metabolic stress, IAPP and islet amyloid

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

Producción científica: Artículo en revista indizadaArtículorevisión exhaustiva

79 Citas (Scopus)

Resumen

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 originalInglés
Páginas (desde-hasta)68-77
Número de páginas10
PublicaciónDiabetes, Obesity and Metabolism
Volumen14
N.ºSuppl. 3
DOI
EstadoPublicada - oct 2012

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