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Responses of Neonatal Rat Islets to Streptozotocin: Limited B-Cell Regeneration and Hyperglycemia
Abstract
Streptozotocin (SZ) was given to 2-day-old neonatal rats, and, during their subsequent development, the interrelationships between plasma glucose, plasma insulin, pancreatic islet morphology, and hormone content were examined. At 4 days of age, a peak of hyperglycemia was observed (SZ, 349 ± 8 mg/dl versus control (C), 127 ± 2) that was associated with a marked reduction of B-cell numbers (SZ, 26.5 ± 2.6% B-cell per islet versus C, 72.8 ± 0.8%). By 10 days of age the SZ animals became normoglycemic with partial recovery of the B-cell number (SZ, 39.6 ± 2.1% versus C, 64.0 ± 2.6%). By 6 weeks hyperglycemia returned (SZ, 345 ± 5.2 mg/dl versus C, 171 ± 6.2) with B-cell number of the SZ being 72% of the C (SZ, 48.8 ± 2.4% versus C, 67.5 ± 1.5%). This hyperglycemia and reduced B-cell number persisted to at least 13 wk age. Despite a marked reduction of pancreatic insulin content observed during development, there was little effect upon glucagon or somatostatin content. At 6 wk of age, the plasma insulin concentration was only 30% of C, which suggests an insulin secretory defect beyond that which could be accounted for by the modest B-cell reduction. The present study indicates that even though active regeneration of B-celle occurred after early injury, the capacity for ultimate normalization was limited. The resultant moderate reduction in B-cell number may be associated with a functional defect in glucose-stimulated insulin secretion.
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In the citing paper
“we adapted a standard regeneration model that uses a single injection of STZ to lead to a loss of ∼50% of the β-cells (31).”
From Age-Dependent Decline in β-Cell Proliferation Restricts the Capacity of β-Cell Regeneration in Mice (2009) · cites this paper as [31]
In the citing paper
“We used this model for two reasons:1) an increase in β-cell proliferation is observed 7 days after STZ injection that correlates with regeneration of β-cell mass, and 2) the residual β-cell mass is sufficient to maintain blood glucose levels, thus potentially minimizing the role of hyperglycemia in β-cell proliferation and apoptosis.”
From Age-Dependent Decline in β-Cell Proliferation Restricts the Capacity of β-Cell Regeneration in Mice (2009) · cites this paper as [31]
In the citing paper
“We used this model for two reasons:1) an increase in β-cell proliferation is observed 7 days after STZ injection that correlates with regeneration of β-cell mass, and 2) the residual β-cell mass is sufficient to maintain blood glucose levels, thus potentially minimizing the role of hyperglycemia in β-cell proliferation and apoptosis.”
From Age-Dependent Decline in β-Cell Proliferation Restricts the Capacity of β-Cell Regeneration in Mice (2009) · cites this paper as [31]
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Metadata
- Authors
- Bonner-Weir, S., Trent, D. F., Honey, R. N., & Weir, G. C.
- Affiliations
- Division of Endocrinology, Department of Medicine, Medical College of Virginia Richmond, Virginia 23298
- Virginia Commonwealth University Medical Center (US)
- ORCID
- Weir, G C
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 1981-01-01
- Volume
- 30
- Issue
- 1
- Pages
- 64-69
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2157604930
- Cited by
- 324
- References
- 0
- Citations by year
- 2026: 4 · 2025: 1 · 2024: 3 · 2023: 4 · 2022: 1 · 2021: 6 · 2020: 4 · 2019: 11 · 2018: 5 · 2017: 7 · 2016: 5 · 2015: 11 · 2014: 8 · 2013: 17 · 2012: 14
- FWCI
- 5.46
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Keywords
- streptozotocin, neonatal rats, pancreatic islets, beta cell regeneration, hyperglycemia, insulin secretion defect, glucagon, somatostatin, islet development, beta-cell injury
- MeSH terms
- Aging, Animals, Animals, Newborn, Blood Glucose, Body Weight, Eating, Female, Glucagon, Hyperglycemia, Insulin, Islets of Langerhans, Male, Regeneration, Sex Factors, Somatostatin, Streptozocin, Rats
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.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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