β cells persist in T1D pancreata without evidence of ongoing β-cell turnover or neogenesis
Open accessAbstract
Context: The cellular basis of persistent β-cell function in type 1 diabetes (T1D) remains enigmatic. No extensive quantitative β-cell studies of T1D pancreata have been performed to test for ongoing β-cell regeneration or neogenesis. Objective: We sought to determine the mechanism of β-cell persistence in T1D pancreata. Design: We studied T1D (n = 47) and nondiabetic control (n = 59) pancreata over a wide range of ages from the Juvenile Diabetes Research Foundation Network of Pancreatic Organ Donors with Diabetes via high-throughput microscopy. Intervention and Main Outcome Measures: We quantified β-cell mass, β-cell turnover [via Ki-67 and terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL)], islet ductal association, and insulin/glucagon coexpression in T1D and control pancreata. Results: Residual insulin-producing β cells were detected in some (but not all) T1D cases of varying disease duration. Several T1D pancreata had substantial numbers of β cells. Although β-cell proliferation was prominent early in life, it dramatically declined after infancy in both nondiabetic controls and T1D individuals. However, β-cell proliferation was equivalent in control and T1D pancreata. β-cell death (assessed by TUNEL) was extremely rare in control and T1D pancreata. Thus, β-cell turnover was not increased in T1D. Furthermore, we found no evidence of small islet/ductal neogenesis or α-cell to β-cell transdifferentiation in T1D pancreata, regardless of disease duration. Conclusion: Longstanding β-cell function in patients with T1D appears to be largely a result of β cells that persist, without any evidence of attempted β-cell regeneration, small islet/ductal neogenesis, or transdifferentiation from other islet endocrine cell types.
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Analysis of pancreatic sections from individuals with long-term type 1 diabetes shows the presence of residual β cells decades after diagnosis.
“However, analysis of pancreatic sections from individuals with long-term type 1 diabetes show the presence of residual β cells decades after diagnosis.62,63”
From Type 1 diabetes (2018) · cites this paper as [63]
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Islet single-cell transcriptomic profiling during obesity-induced beta cell expansion in female mice
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Self-citationLes cellules MAIT dans le diabète de type 1 chez l'homme
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- Authors
- Lam, C. J., Jacobson, D. R., Rankin, M. M., Cox, A. R., & Kushner, J. A.
- Affiliations
- Baylor College of Medicine (US)
- Children's Hospital of Philadelphia (US)
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2017-02-27
- Volume
- 102
- Issue
- 8
- Pages
- 2647-2659
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- PMC
- PMC5546851
- OpenAlex
- W2742483070
- Cited by
- 68
- References
- 40
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 6 · 2023: 8 · 2022: 7 · 2021: 15 · 2020: 3 · 2019: 9 · 2018: 10 · 2017: 1
- FWCI
- 6.44
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (R01AG040110)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK079638)
- 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 Management and Research
- Keywords
- type 1 diabetes, pancreatic beta cells, beta-cell turnover, beta-cell proliferation, beta-cell death, islet neogenesis, beta-cell mass, disease duration
- MeSH terms
- Adolescent, Adult, Aged, Child, Child, Preschool, Diabetes Mellitus, Type 1, Female, Glucagon, Humans, Infant, Infant, Newborn, Insulin, Islets of Langerhans, Male, Middle Aged, Pancreas, Regeneration, Time Factors, Case-Control Studies, Ki-67 Antigen, In Situ Nick-End Labeling, Glucagon-Secreting Cells, Insulin-Secreting Cells, Cell Transdifferentiation, Young Adult
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