ReviewEndocrine reviews2008
Islet amyloid in type 2 diabetes, and the toxic oligomer hypothesis.
Review in Endocrine reviews, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 270 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
270 citing papers in PubMed, 599 citations in OpenAlex.
- Trial
- The dawn phenomenon in diabetes: pathophysiology from periphery to central nervous system and circadian rhythm-based therapeutic strategies.Acta diabetologica · 2026Review
- Insulin resistance induced by pesticides is overcome by pancreatic islet adaptation in a mouse model of Parkinson's disease.Molecular metabolism · 2026Article
- QBP1 Peptide as a Potential Anti-Amyloidogenic Therapy for Type 2 Diabetes: An In Vitro Study.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Janus Polymeric Nanorods Inhibit human Amylin Oligomerization and Fibrillation for Potential Type 2 Diabetes Treatment.Small science · 2026Article
- Use of Small Organic Molecules to Improve Pancreatic Beta Cell Resilience to IAPP-Induced Proteotoxic Stress.International journal of molecular sciences · 2026Review
- Explainable AI-based analysis of human pancreas sections identifies traits of type 2 diabetes.Nature communications · 2026Article
- A structural model of toxic amyloid oligomers involved in type 2 diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- SATB1 Exhibits a Protective Role in HAmylin-Oligomer-Induced Neuronal Damage and Cognition Decline.CNS neuroscience & therapeutics · 2026Article
- Resveratrol modulates pancreatic proteotoxic stress and metabolic dysfunction in human IAPP transgenic mice.Frontiers in endocrinology · 2026Article
- Review
- Inhibition of Human Amylin Aggregation:ACS omega · 2025Article
- The role of hydrophobic collapse in cytotoxic and functional amyloid oligomerization.Biophysical journal · 2025Article
- Amylin: emergent therapeutic opportunities in overweight, obesity and diabetes mellitus.Nature reviews. Endocrinology · 2025Review
- Chemical synthesis uncovers the significant impact of natural glycosylation on islet amyloid polypeptide aggregation.Science advances · 2025Article
- Identifying the Role of Individual Seal IAPP Amino Acids in Inhibiting the Aggregation of Human IAPP.Protein and peptide letters · 2025Article
- 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
- Type 2 diabetes mellitus in adults: pathogenesis, prevention and therapy.Signal transduction and targeted therapy · 2024 · on this mapReview
- IAPP - oligomerisation levels in plasma of people with type 2 diabetes.Scientific reports · 2024Article
- Differential effects of ganglioside lipids on the conformation and aggregation of islet amyloid polypeptide.Protein science : a publication of the Protein Society · 2024Article
210 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Type 2 diabetes (T2DM) is characterized by insulin resistance, defective insulin secretion, loss of beta-cell mass with increased beta-cell apoptosis and islet amyloid. The islet amyloid is derived from islet amyloid polypeptide (IAPP, amylin), a protein coexpressed and cosecreted with insulin by pancreatic beta-cells. In common with other amyloidogenic proteins, IAPP has the propensity to form membrane permeant toxic oligomers. Accumulating evidence suggests that these toxic oligomers, rather than the extracellular amyloid form of these proteins, are responsible for loss of neurons in neurodegenerative diseases. In this review we discuss emerging evidence to suggest that formation of intracellular IAPP oligomers may contribute to beta-cell loss in T2DM. The accumulated evidence permits the amyloid hypothesis originally developed for neurodegenerative diseases to be reformulated as the toxic oligomer hypothesis. However, as in neurodegenerative diseases, it remains unclear exactly why amyloidogenic proteins form oligomers in vivo, what their exact structure is, and to what extent these oligomers play a primary or secondary role in the cytotoxicity in what are now often called unfolded protein diseases.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.