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Impaired islet turnover in human donor pancreata with aging
Abstract
Objective: The prevalence of type 2 diabetes mellitus escalates with aging although β-cell mass, a primary parameter of β-cell function, is subject to compensatory regulation. So far it is unclear whether the proliferative capacity of pancreatic islets is restricted by senescence. Materials and methods: Human pancreatic tissue from n=20 non-diabetic organ donors with a mean age of 50.2±3.5 years (range 7–66 years) and mean body mass index of 25.7±0.9 kg/m 2 (17.2–33.1 kg/m 2) was morphometrically analyzed to determine β-cell volume, β-cell replication, β-cell apoptosis, islet neogenesis, and pancreatic duodenal homeobox-1 (PDX-1) expression. Results: Relative β-cell volume in human pancreata (mean 2.3±0.2%) remains constant with aging (r=0.26, P=ns). β-cell replication (r=0.71, P=0.0004) decreases age-dependently, while β-cell apoptosis does not change significantly (r=0.42, P=0.08). Concomitantly, PDX-1 expression is downregulated with age in human pancreatic tissue (r=0.65, P=0.002). The rate of islet neogenesis is not affected by aging (r=0.13, P=ns). Conclusions: In non-diabetic humans, aging is linked with impaired islet turnover possibly due to reduced PDX-1 expression. As β-cell replication is considered to be the main mechanism responsible for β-cell regeneration, these changes restrict the flexibility of the aging human pancreas to adapt to changing demands for insulin secretion and increase the risk for the development of diabetes mellitus in older subjects.
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“However, age-related declines of pancreatic islet function4, 14 and of islet proliferative capacity15, 16; have been described.”
From Diabetes in Older Adults: A Consensus Report (2012) · cites this paper as [14]
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Metadata
- Authors
- Reers, C., Erbel, S., Esposito, I., Schmied, B., Büchler, M. W., Nawroth, P. P., & Ritzel, R. A.
- Affiliations
- Heidelberg University (DE)
- Corresponding author
- Ritzel, Robert A
- Venue
- European Journal of Endocrinology
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-02
- Volume
- 160
- Issue
- 2
- Pages
- 185-191
- ISSN
- 0804-4643 (ISSN-L)
- 1479-683X
- OpenAlex
- W2164058944
- Cited by
- 113
- References
- 33
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 4 · 2023: 3 · 2022: 5 · 2021: 8 · 2020: 6 · 2019: 4 · 2018: 2 · 2017: 7 · 2016: 8 · 2015: 7 · 2014: 9 · 2013: 16 · 2012: 12
- FWCI
- 4.92
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- European Journal of Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
- Site cant be reached (submittedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › 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
- aging, beta-cell proliferation, beta-cell apoptosis, islet neogenesis, beta-cell mass, beta cell regeneration, type 2 diabetes risk, human pancreas, organ donors
- MeSH terms
- Adolescent, Adult, Aged, Aging, Cell Division, Child, Diabetes Mellitus, Type 2, Female, Glucagon, Humans, Insulin, Islets of Langerhans, Male, Middle Aged, Risk Factors, Tissue Donors, Trans-Activators, Prevalence, Cellular Senescence, Homeodomain Proteins, Insulin-Secreting Cells, Young Adult
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