Cellular composition of the human diabetic pancreas
Open accessAbstract
Insulin, glucagon, somatostatin and pancreatic polypeptide cells were stained by immunoperoxidase techniques and quantitated morphometrically in sections of pancreases obtained from eight control subjects, four Type 1 (insulin-dependent) and eight Type 2 (non-insulin-dependent) diabetic patients. The whole pancreas was studied to take into consideration the heterogeneous distribution of the different cell types. From the volume density of each cell type, and the weight of each lobe of the pancreas, the total mass of endocrine tissue was calculated. It averaged 1395 mg in control subjects, 413 mg in Type 1 and 1449 mg in Type 2 diabetic patients. The loss of endocrine tissue observed in the Type 1 patients was almost restricted to the lobe poor in pancreatic polypeptide cells. In these patients, B cells were practically absent (at the most seven per section), but the 'atrophic islets' still contained numerous A, D, or pancreatic polypeptide cells. The mass of A, D and pancreatic polypeptide cells and the ratio of D to A cells were not different from those measured in the control subjects. This shows that the disappearance of B cells in Type 1 diabetes has no preferential effect on any other endocrine cell of the pancreas. In Type 2 diabetes, the mass of A cells was increased, whereas that of B, D and pancreatic polypeptide cells was not changed. This hyperplasia of A cells leads to a decrease in the ratio of B to A and of D to A cells. These alterations may enlighten certain aspects of the physiopathology of Type 2 diabetes.
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Type-1 diabetes onset results in a dramatic decrease in islet insulin content but only marginally affects glucagon and somatostatin contents.
“T1D onset resulted in a dramatic decrease in islet insulin content but only marginally affected glucagon and somatostatin contents (Extended Data Fig. 2a–c), in agreement with human histological data11.”
From Loss of electrical β-cell to δ-cell coupling underlies impaired hypoglycaemia-induced glucagon secretion in type-1 diabetes (2024) · cites this paper as [11]
Reports suggest delta-cell number is increased in diabetes, while other studies suggest the number is unaltered in patients' islets.
“Although there have been reports suggesting that the delta-cell number is increased in diabetes, other studies suggested that the number of these cells was unaltered in patients’ islets.153,154”
From A review of current trends with type 2 diabetes epidemiology, aetiology, pathogenesis, treatments and future perspectives (2021) · cites this paper as [154]
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- Authors
- Rahier, J., Goebbels, R. M., & Henquin, J. C.
- Affiliations
- Cliniques Universitaires Saint-Luc (BE)
- UCLouvain (BE)
- Venue
- Diabetologia
- Published
- 1983-05
- Volume
- 24
- Issue
- 5
- Pages
- 366-71
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W1975799894
- Cited by
- 395
- References
- 32
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 10 · 2023: 5 · 2022: 5 · 2021: 11 · 2020: 8 · 2019: 12 · 2018: 10 · 2017: 11 · 2016: 17 · 2015: 19 · 2014: 20 · 2013: 8 · 2012: 13
- FWCI
- 14.68
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Digital Access to Libraries (submittedVersion)
- Funders
- Fonds De La Recherche Scientifique - FNRS
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- pancreatic endocrine cells, type 1 diabetes, type 2 diabetes, beta cell destruction, alpha cell hyperplasia, delta cells, pancreatic polypeptide cells, insulin, glucagon, somatostatin, islet atrophy
- MeSH terms
- Adolescent, Adult, Aged, Diabetes Mellitus, Female, Histocytochemistry, Humans, Immunoenzyme Techniques, Insulin, Islets of Langerhans, Male, Middle Aged
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