Metabolic stress, IAPP and islet amyloid
| Autor: | Clara Westwell-Roper, Joel Montane, C. Bruce Verchere, Kathryn J. Potter, Agnieszka M. Klimek-Abercrombie |
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| Rok vydání: | 2012 |
| Předmět: |
endocrine system
medicine.medical_specialty Amyloid Endocrinology Diabetes and Metabolism medicine.medical_treatment Amylin Apoptosis Type 2 diabetes Islets of Langerhans Endocrinology Insulin resistance Stress Physiological Internal medicine Internal Medicine medicine Animals Humans Proinsulin geography geography.geographical_feature_category business.industry Pancreatic islets Insulin Islet medicine.disease Islet Amyloid Polypeptide Rats medicine.anatomical_structure Diabetes Mellitus Type 2 Hyperglycemia Insulin Resistance business |
| Zdroj: | Diabetes, Obesity and Metabolism. 14:68-77 |
| ISSN: | 1462-8902 |
| DOI: | 10.1111/j.1463-1326.2012.01657.x |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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