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Study · Animal study (in vivo) · rat · 2003

4 results

Neonatal exendin-4 prevents the development of diabetes in the intrauterine growth retarded rat.

Stoffers DA, Desai BM, DeLeon DD, Simmons RA

Diabetes1 Mar 2003Cited by 188 (Europe PMC)

PMID12606515 (opens in a new tab)DOI10.2337/diabetes.52.3.734 (opens in a new tab)PepBankPUB-12606515
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study4

4 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In intrauterine growth-retarded rats, neonatal exendin‑4 prevented diabetes development.

    In plain wordsIn rats with restricted fetal growth, neonatal exendin‑4 prevented diabetes development.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseDiabetes development
    Study

    ratn: not reported in source

    intrauterine growth-retarded rats
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We show here that administration of a pancreatic beta-cell trophic factor, exendin-4 (Ex-4), during the prediabetic neonatal period dramatically prevents the development of diabetes in this model.
    1 context sentence
    Summary · context
    Therefore, a rat model of uteroplacental insufficiency was developed; intrauterine growth-retarded (IUGR) rats develop diabetes with a phenotype similar to that observed in the human with type 2 diabetes.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In intrauterine growth-retarded rats, neonatal exendin‑4 prevented the progressive loss of insulin-producing beta-cell mass.

    In plain wordsIn rats with restricted fetal growth, neonatal exendin‑4 prevented progressive loss of insulin-producing cells.

    Peptide
    Exenatide (exendin-4)
    Outcome
    IncreaseInsulin-producing beta-cell mass
    Study

    ratn: not reported in source

    intrauterine growth-retarded rats
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    This occurs because neonatal Ex-4 prevents the progressive reduction in insulin-producing beta-cell mass that is observed in IUGR rats over time.
    1 context sentence
    Summary · context
    Therefore, a rat model of uteroplacental insufficiency was developed; intrauterine growth-retarded (IUGR) rats develop diabetes with a phenotype similar to that observed in the human with type 2 diabetes.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In intrauterine growth-retarded rats, neonatal exendin‑4 restored PDX expression to normal levels.

    In plain wordsIn rats with restricted fetal growth, neonatal exendin‑4 restored normal PDX expression.

    Peptide
    Exenatide (exendin-4)
    Outcome
    Not applicablePDX expression
    Study

    ratn: not reported in source

    intrauterine growth-retarded rats
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Expression of PDX, a critical regulator of pancreas development and islet differentiation, is restored to normal levels, and islet beta-cell proliferation rates are normalized by the neonatal Ex-4 treatment.
    1 context sentence
    Summary · context
    Therefore, a rat model of uteroplacental insufficiency was developed; intrauterine growth-retarded (IUGR) rats develop diabetes with a phenotype similar to that observed in the human with type 2 diabetes.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In intrauterine growth-retarded rats, neonatal exendin‑4 normalized islet beta-cell proliferation rates.

    In plain wordsIn rats with restricted fetal growth, neonatal exendin‑4 normalized insulin-producing cell proliferation.

    Peptide
    Exenatide (exendin-4)
    Outcome
    Not applicableIslet beta-cell proliferation
    Study

    ratn: not reported in source

    intrauterine growth-retarded rats
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Expression of PDX, a critical regulator of pancreas development and islet differentiation, is restored to normal levels, and islet beta-cell proliferation rates are normalized by the neonatal Ex-4 treatment.
    1 context sentence
    Summary · context
    Therefore, a rat model of uteroplacental insufficiency was developed; intrauterine growth-retarded (IUGR) rats develop diabetes with a phenotype similar to that observed in the human with type 2 diabetes.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    22 Oct 2026, 02:26 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 18:59 UTC

    First added · source update from Europe PMC

Subjects

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