β‐cell mass in people with type 2 diabetes
Open accessAbstract
The early occurrence of β‐cell dysfunction has been broadly recognized as a critical determinant of the development and progression of type 2 diabetes. β‐cell dysfunction might be induced by insufficient β‐cell mass, by a dysfunction of the β‐cells, or both. Whether or not β‐cell dysfunction constitutes a cause of reduced β‐cells or vice‐versa currently remains unclear. The results of some studies have measured the loss of β‐cells in type 2 diabetic patients at between 22 and 63% by planimetric measurements. Because β‐cell hypertrophy has been noted in type 2 diabetic patients, the loss of β‐cell number should prove more profound than what has thus far been reported. Furthermore, β‐cell volumes are reduced even in patients with impaired fasting glucose. Such defects in β‐cell mass are associated with increased apoptosis rather than insufficient replication or neogenesis of β‐cells. With these results, although they still require clarification, the peak β‐cell mass might be determined at quite an early stage of life, and then might decline progressively over time as the result of exposure to harmful environmental influences over one’s lifetime. In this review, we have summarized the relevant studies regarding β‐cell mass in patients with type 2 diabetes, and then presented a review of the various causes of β‐cell loss in adults. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.00072.x, 2010)
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Given the reduced population of islet beta-cells in T2D patients, enhanced proliferation would in theory be desirable to increase plasma insulin levels and promote normoglycaemia and normolipidaemia.
“Given the reduced population of these cells in patients,310 enhanced proliferation would, in theory, be desirable to increase plasma insulin levels in patients to promote normoglycaemia and normolipidaemia.”
From A review of current trends with type 2 diabetes epidemiology, aetiology, pathogenesis, treatments and future perspectives (2021) · cites this paper as [310]
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- Authors
- Cho, J., Kim, J., Shin, J., Shin, J., & Yoon, K.
- Affiliations
- The Catholic University of Korea Seoul St. Mary's Hospital (KR)
- Corresponding author
- Yoon, Kun‐Ho
- Venue
- Journal of Diabetes Investigation
- Publisher
- Wiley
- Published
- 2010-11-22
- Volume
- 2
- Issue
- 1
- Pages
- 6-17
- ISSN
- 2040-1116 (ISSN-L)
- 2040-1124
- PMC
- PMC4008010
- OpenAlex
- W2163505408
- Cited by
- 69
- References
- 109
- Citations by year
- 2025: 6 · 2024: 2 · 2023: 7 · 2022: 7 · 2021: 10 · 2020: 8 · 2019: 6 · 2018: 7 · 2017: 5 · 2016: 2 · 2015: 3 · 2013: 3 · 2012: 1
- FWCI
- 0.34
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Diabetes Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- 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
- beta-cell mass, type 2 diabetes, beta-cell dysfunction, beta cell destruction, beta-cell apoptosis, beta-cell hypertrophy, beta-cell neogenesis, impaired fasting glucose, planimetry
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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