Cited by 220Pancreatic function and diabetesDiabetes and associated disordersDiabetes Treatment and Management

Linear correlation between beta-cell mass and body weight throughout the lifespan in Lewis rats: role of beta-cell hyperplasia and hypertrophy.

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Montanya, E, Nacher, V, Biarnés, M, Soler, J·2000·Diabetes

Abstract

We determined the beta-cell replicative rate, beta-cell apoptosis, cross-sectional beta-cell area, and pancreatic beta-cell mass throughout the entire postweaning lifespan (months 1, 3, 7, 10, 15, and 20) of Lewis rats. Beta-cell replication was progressively reduced in the initial months of life but remained stable after month 7 (month 1, 0.99 +/- 0.10%; month 3, 0.24 +/- 0.04%; month 7, 0.12 +/- 0.02%; month 10, 0.14 +/- 0.02%; month 15, 0.10 +/- 0.03%; month 20, 0.13 +/- 0.03%; analysis of variance [ANOVA], P < 0.001). Beta-cell apoptosis was low and did not change significantly from month 1 to 20 of life. Cross-sectional area of individual beta-cells increased progressively in the initial months, remained stable from month 7 to 15, and increased again on month 20. The estimated number of beta-cells per pancreas, calculated as the ratio of total beta-cell mass to individual beta-cell mass, tripled from month 1 to 7 but did not change significantly thereafter. Beta-cell mass increased approximately 8 times from month 1 to 20 (month 1, 2.04 +/- 0.28 mg; month 20, 15.5 +/- 2.32 mg; ANOVA, P < 0.001) and showed a strong and significant linear correlation with body weight (r = 0.98, P < 0.001). In summary, we have shown that beta-cell replication was maintained throughout the lifespan in normal rats, clearly establishing that the beta-cell birth rate does not fall to 0, even in very old rats. Beta-cell mass increased throughout the lifespan, closely matching the increment in total body weight at any time point. This increment was selective for beta-cells, since the growth of the endocrine non-beta-cell mass was limited to the initial months of life. Both beta-cell hypertrophy and hyperplasia contributed to increased beta-cell mass in young animals, but only beta-cell hypertrophy was responsible for the increased beta-cell mass found in old animals. This study provides a global perspective for understanding the dynamics of beta-cell mass in young, adult, and aged animals.

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  1. [12]12. Hellerstrom C, Swenne I, Andersson A: Islet replication and diabetes. In The Pathology of the Endocrine Pancreas in Diabetes. Lefebvre PJ, Pipeleers DG, Eds. Berlin, Springer-Verlag, 1988, p. 141-170

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Authors
Montanya, E., Nacher, V, Biarnés, M., & Soler, J.
Affiliations
Bellvitge University Hospital (ES)
Venue
Diabetes
Published
2000-08-01
Volume
49
Issue
8
Pages
1341-1346
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
OpenAlex
W2097735638
Cited by
220
References
34
Citations by year
2026: 1 · 2025: 3 · 2024: 3 · 2023: 7 · 2022: 6 · 2021: 7 · 2020: 7 · 2019: 4 · 2018: 6 · 2017: 9 · 2016: 8 · 2015: 13 · 2014: 6 · 2013: 7 · 2012: 14
FWCI
9.00
Type
journal article
Language
en
Open access
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
  • RECERCAT (Consorci de Serveis Universitaris de Catalunya) (acceptedVersion, other-oa)
  • Dipòsit Digital de la Universitat de Barcelona (Universitat de Barcelona) (submittedVersion, cc-by-nc-nd)
Funders
Ministerio de Sanidad, Consumo y Bienestar Social
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, beta-cell hyperplasia, beta-cell hypertrophy, beta-cell proliferation, beta-cell apoptosis, body weight, lifespan, aging, pancreatic beta cells, Lewis rats
MeSH terms
Aging, Animals, Blood Glucose, Body Weight, Cell Division, Hyperplasia, Hypertrophy, Islets of Langerhans, Male, Organ Size, Rats, Inbred Lew, Apoptosis, Rats

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