The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
Persistent Improvement of Type 2 Diabetes in the Goto-Kakizaki Rat Model by Expansion of the β-Cell Mass During the Prediabetic Period With Glucagon-Like Peptide-1 or Exendin-4
Open accessAbstract
In the Goto-Kakizaki (GK) rat, a genetic model of type 2 diabetes, the neonatal β-cell mass deficit is considered to be the primary defect leading to basal hyperglycemia, which is detectable for the first time 3 weeks after birth. We investigated in GK females the short- and the long-term effects of a treatment with glucagon-like peptide-1 (GLP-1) or its long-acting analog exendin-4 (Ex-4) during the first postnatal week (during the prediabetic period). GK rats were treated with daily injections of glucagon-like peptide-1 (400 μg · kg−1 · day−1) or Ex-4 (3 μg · kg−1 · day−1) from day 2 to day 6 after birth and were evaluated against Wistar and untreated GK rats. Under these conditions, on day 7 both treatments enhanced pancreatic insulin content and total β-cell mass by stimulating β-cell neogenesis and regeneration. Follow-up of biological characteristics from day 7 to adult age (2 months) showed that such a GLP-1 or Ex-4 treatment exerted long-term favorable influences on β-cell mass and glycemic control at adult age. As compared to untreated GK rats, 2-month-old treated rats exhibited significantly decreased basal plasma glucose. Their glucose-stimulated insulin secretion, in vivo after intravenous glucose load or in vitro using isolated perfused pancreas, was slightly improved. This contributed at least partly to improve the in vivo plasma glucose disappearance rate, which was found to be increased in both treated GK groups compared to the untreated GK group. These findings in the GK model indicated, for the first time, that GLP-1 or Ex-4 treatment limited to the prediabetic period delays the installation and limits the severity of type 2 diabetes. Under these conditions, GLP-1 represents a unique tool because of its β-cell replenishing effect in spontaneously diabetic rodents. It may prove to be an invaluable agent for the prevention of human type 2 diabetes.
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Dynamics of β-cell Mass in the Growing Rat Pancreas: Estimation With a Simple Mathematical Model
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Cited by
The Physiology of Glucagon-like Peptide 1
Holst, J. J. (2007) · Physiological Reviews · doi:10.1152/physrev.00034.2006 · Cited by 3,371
Farilla, L., Bulotta, A., Hirshberg, B., Li Calzi, S., Khoury, N., Noushmehr, H., Bertolotto, C., Di Mario, U., Harlan, D. M., & Perfetti, R. (2003) · Endocrinology · doi:10.1210/en.2003-0323 · Cited by 664
Enhancing Incretin Action for the Treatment of Type 2 Diabetes
Drucker, D. J. (2003) · Diabetes Care · doi:10.2337/diacare.26.10.2929 · Cited by 579
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Metadata
- Authors
- Tourrel, C., Bailbe, D., Lacorne, M., Meile, M.-J., Kergoat, M., & Portha, B.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2002-05-01
- Volume
- 51
- Issue
- 5
- Pages
- 1443-1452
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2109069837
- Cited by
- 285
- References
- 32
- FWCI
- 15.73
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Persistent Improvement of Type 2 Diabetes in the Goto-Kakizaki Rat Model by Expansion of the β-Cell Mass During the Prediabetic Period With Glucagon-Like Peptide-1 or Exendin-4. https://app.cochat.ai/papers/10.2337/diabetes.51.5.1443
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- Tourrel, C., Bailbe, D., Lacorne, M., Meile, M.-J., Kergoat, M., & Portha, B. (2002). Persistent Improvement of Type 2 Diabetes in the Goto-Kakizaki Rat Model by Expansion of the β-Cell Mass During the Prediabetic Period With Glucagon-Like Peptide-1 or Exendin-4. Diabetes. https://doi.org/10.2337/diabetes.51.5.1443
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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