ArticleThe Journal of biological chemistry2011
Involvement of ATP-sensitive potassium (K(ATP)) channels in the loss of beta-cell function induced by human islet amyloid polypeptide.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- QBP1 Peptide as a Potential Anti-Amyloidogenic Therapy for Type 2 Diabetes: An In Vitro Study.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A new form of diabetes caused by INS mutations defined by zygosity, stem cell and population data.EMBO molecular medicine · 2026Article
- Resveratrol protects pancreatic beta cell and hippocampal cells from the aggregate-prone capacity of hIAPP.Scientific reports · 2024Article
- The overexpression of human amylin in pancreatic β cells facilitate the appearance of amylin aggregates in the kidney contributing to diabetic nephropathy.Scientific reports · 2024Article
- The potential role of human islet amyloid polypeptide in type 2 diabetes mellitus and Alzheimer's diseases.Diabetology & metabolic syndrome · 2023Review
- Contribution of Mitochondria to Insulin Secretion by Various Secretagogues.Antioxidants & redox signaling · 2022Review
- Urolithin B: Two-way attack on IAPP proteotoxicity with implications for diabetes.Frontiers in endocrinology · 2022Article
- Human Islet Amyloid Polypeptide Overexpression in INS-1E Cells Influences Amylin Oligomerization under ER Stress and Oxidative Stress.International journal of molecular sciences · 2021Article
- 4-Phenylbutyrate (PBA) treatment reduces hyperglycemia and islet amyloid in a mouse model of type 2 diabetes and obesity.Scientific reports · 2021Article
- The Pancreatic β-Cell: The Perfect Redox System.Antioxidants (Basel, Switzerland) · 2021Review
- Article
- Insulin Resistance in Osteoarthritis: Similar Mechanisms to Type 2 Diabetes Mellitus.Journal of nutrition and metabolism · 2020Review
- A Novel Pentapeptide Inhibitor Reduces Amyloid Deposit Formation by Direct Interaction with hIAPP.International journal of endocrinology · 2019Article
- Membranes as modulators of amyloid protein misfolding and target of toxicity.Biochimica et biophysica acta. Biomembranes · 2018Review
- Pancreatic β cells overexpressing hIAPP impaired mitophagy and unbalanced mitochondrial dynamics.Cell death & disease · 2018Article
- Conformational switching within dynamic oligomers underpins toxic gain-of-function by diabetes-associated amyloid.Nature communications · 2018Article
- Amyloid-induced β-cell dysfunction and islet inflammation are ameliorated by 4-phenylbutyrate (PBA) treatment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- BACE2 suppression promotes β-cell survival and function in a model of type 2 diabetes induced by human islet amyloid polypeptide overexpression.Cellular and molecular life sciences : CMLS · 2017Article
- A gut-brain neural circuit controlled by intestinal gluconeogenesis is crucial in metabolic health.Molecular metabolism · 2015Article
- On the Environmental Factors Affecting the Structural and Cytotoxic Properties of IAPP Peptides.Journal of diabetes research · 2015Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Islet amyloid polypeptide (IAPP) is a major component of amyloid deposition in pancreatic islets of patients with type 2 diabetes. It is known that IAPP can inhibit glucose-stimulated insulin secretion; however, the mechanisms of action have not yet been established. In the present work, using a rat pancreatic beta-cell line, INS1E, we have created an in vitro model that stably expressed human IAPP gene (hIAPP cells). These cells showed intracellular oligomers and a strong alteration of glucose-stimulated insulin and IAPP secretion. Taking advantage of this model, we investigated the mechanism by which IAPP altered beta-cell secretory response and contributed to the development of type 2 diabetes. We have measured the intracellular Ca(2+) mobilization in response to different secretagogues as well as mitochondrial metabolism. The study of calcium signals in hIAPP cells demonstrated an absence of response to glucose and also to tolbutamide, indicating a defect in ATP-sensitive potassium (K(ATP)) channels. Interestingly, hIAPP showed a greater maximal respiratory capacity than control cells. These data were confirmed by an increased mitochondrial membrane potential in hIAPP cells under glucose stimulation, leading to an elevated reactive oxygen species level as compared with control cells. We concluded that the hIAPP overexpression inhibits insulin and IAPP secretion in response to glucose affecting the activity of K(ATP) channels and that the increased mitochondrial metabolism is a compensatory response to counteract the secretory defect of beta-cells.
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