ArticleThe journal of pathology. Clinical research2019
Characterisation of the endocrine pancreas in type 1 diabetes: islet size is maintained but islet number is markedly reduced.
Article in The journal of pathology. Clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Deep learning-powered quantification of endocrine cells and CD3Diabetologia · 2026Article
- Integrated histopathology of the human pancreas throughout stages of type 1 diabetes progression.Nature communications · 2026Article
- Cells Co-Producing Insulin and Glucagon in Congenital Hyperinsulinism.Life (Basel, Switzerland) · 2025Article
- 3D imaging of human pancreas suggests islet size and endocrine composition influence their loss in type 1 diabetes.Nature communications · 2025Article
- Small things matter: Lack of extraislet β cells in type 1 diabetes.Science advances · 2025Article
- Sweating the Small Stuff: A Closer Look at the Endocrine Pancreas Throughout Stages of Type 1 Diabetes Progression.Diabetes · 2025Article
- Islet delta-cell architecture is remodelled in the human pancreas during type 1 diabetes.Scientific reports · 2025Article
- 3D imaging of human pancreas suggests islet sizeand endocrine composition influence their loss intype 1 diabetes.Research square · 2025Article
- 3D imaging of human pancreas suggests islet size and endocrine composition influence their loss in type 1 diabetes.bioRxiv : the preprint server for biology · 2025Article
- Scaffold-free endocrine tissue engineering: role of islet organization and implications in type 1 diabetes.BMC endocrine disorders · 2025Review
- Loss of insulin-expressing extra-islet cells in type 1 diabetes is accompanied with increased number of glucagon-expressing extra-islet cells.Virchows Archiv : an international journal of pathology · 2025Article
- Integrated histopathology of the human pancreas throughout stages of type 1 diabetes progression.bioRxiv : the preprint server for biology · 2025Article
- Detection of Insulin in Insulin-Deficient Islets of Patients with Type 1 Diabetes.Life (Basel, Switzerland) · 2025Article
- Extra-islet cells expressing insulin or glucagon in the pancreas of young organ donors.Acta diabetologica · 2024Article
- Bridging the Gap: Pancreas Tissue Slices From Organ and Tissue Donors for the Study of Diabetes Pathogenesis.Diabetes · 2024Review
- Beta cell dedifferentiation in type 1 diabetes: sacrificing function for survival?Frontiers in endocrinology · 2024Article
- Optimized protocol for shotgun label-free proteomic analysis of pancreatic islets.Biology methods & protocols · 2024Review
- Review
- Pancreatic Pathological Changes in Murine Toxoplasmosis and Possible Association with Diabetes Mellitus.Biomedicines · 2022Article
- Pregnancy induces pancreatic insulin secretion in women with long-standing type 1 diabetes.BMJ open diabetes research & care · 2022Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin deficiency in type 1 diabetes (T1D) is generally considered a consequence of immune-mediated specific beta-cell loss. Since healthy pancreatic islets consist of ~65% beta cells, this would lead to reduced islet size, while the number of islets per pancreas volume (islet density) would not be affected. In this study, we compared the islet density, size, and size distribution in biopsies from subjects with recent-onset or long-standing T1D, with that in matched non-diabetic subjects. The results presented show preserved islet size and islet size distribution, but a marked reduction in islet density in subjects with recent onset T1D compared with non-diabetic subjects. No further reduction in islet density occurred with increased disease duration. Insulin-negative islets in T1D subjects were dominated by glucagon-positive cells that often had lost the alpha-cell transcription factor ARX while instead expressing PDX1, normally only expressed in beta cells within the islets. Based on our findings, we propose that failure to establish a sufficient islet number to reach the beta-cell mass needed to cope with episodes of increased insulin demand contributes to T1D susceptibility. Exhaustion induced by relative lack of beta cells could then potentially drive beta-cell dedifferentiation to alpha-cells, explaining the preserved islet size observed in T1D compared to controls.
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