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Study · Animal study (in vivo) · rat · 2011

9 results

Exendin-4 increases histone acetylase activity and reverses epigenetic modifications that silence Pdx1 in the intrauterine growth retarded rat.

Pinney SE, Jaeckle Santos LJ, Han Y, Stoffers DA, Simmons RA

Diabetologia21 Jul 2011Cited by 95 (Europe PMC)

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 study9

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In IUGR rats, exendin‑4 increased USF1 phosphorylation in islets.

    In plain wordsIn rats with restricted fetal growth, exendin‑4 increased USF1 phosphorylation in islets.

    Outcome
    IncreaseUSF1 phosphorylation
    Study

    ratn: not reported in source

    Intrauterine growth retardation
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated · postnatal days 1-6As given in this study (rat).

    Source sentences

    Summary
    Phosphorylation of USF1 was markedly increased in IUGR islets in Ex-4 treated animals.
    1 context sentence
    Summary · context
    IUGR was induced by bilateral uterine artery ligation in fetal life. Ex-4 was given on postnatal days 1-6 of life. Islets were isolated at 1 week and at 3-12 months.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In IUGR rat islets, exendin‑4 increased USF1 association at the Pdx1 promoter.

    In plain wordsIn rats with restricted fetal growth, exendin‑4 increased USF1 binding at the Pdx1 promoter.

    Outcome
    IncreaseUSF1 promoter association
    Study

    ratn: not reported in source

    Intrauterine growth retardation
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated · postnatal days 1-6As given in this study (rat).

    Source sentences

    Summary
    This resulted in increased USF1 and PCAF association at the proximal promoter of Pdx1, thereby increasing histone acetyl transferase (HAT) activity.
    1 context sentence
    Summary · context
    IUGR was induced by bilateral uterine artery ligation in fetal life. Ex-4 was given on postnatal days 1-6 of life. Islets were isolated at 1 week and at 3-12 months.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In IUGR rat islets, exendin‑4 increased PCAF association at the Pdx1 promoter.

    In plain wordsIn rats with restricted fetal growth, exendin‑4 increased PCAF binding at the Pdx1 promoter.

    Outcome
    IncreasePCAF promoter association
    Study

    ratn: not reported in source

    Intrauterine growth retardation
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated · postnatal days 1-6As given in this study (rat).

    Source sentences

    Summary
    This resulted in increased USF1 and PCAF association at the proximal promoter of Pdx1, thereby increasing histone acetyl transferase (HAT) activity.
    1 context sentence
    Summary · context
    IUGR was induced by bilateral uterine artery ligation in fetal life. Ex-4 was given on postnatal days 1-6 of life. Islets were isolated at 1 week and at 3-12 months.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In IUGR rat islets, exendin‑4 increased histone acetyl transferase activity.

    In plain wordsIn rats with restricted fetal growth, exendin‑4 increased histone acetyl transferase activity in islets.

    Outcome
    IncreaseHistone acetyl transferase activity
    Study

    ratn: not reported in source

    Intrauterine growth retardation
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated · postnatal days 1-6As given in this study (rat).

    Source sentences

    Summary
    This resulted in increased USF1 and PCAF association at the proximal promoter of Pdx1, thereby increasing histone acetyl transferase (HAT) activity.
    1 context sentence
    Summary · context
    IUGR was induced by bilateral uterine artery ligation in fetal life. Ex-4 was given on postnatal days 1-6 of life. Islets were isolated at 1 week and at 3-12 months.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In IUGR rat islets, exendin‑4 permanently increased histone H3 acetylation at the Pdx1 promoter.

    In plain wordsIn rats with restricted fetal growth, exendin‑4 permanently increased histone H3 acetylation at the Pdx1 promoter.

    Outcome
    IncreaseHistone H3 acetylation
    Study

    ratn: not reported in source

    Intrauterine growth retardation
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated · postnatal days 1-6As given in this study (rat).

    Source sentences

    Summary
    Histone H3 acetylation and trimethylation of H3K4 were permanently increased, whereas Dnmt1 binding and subsequent DNA methylation were prevented at the proximal promoter of Pdx1 in IUGR islets.
    1 context sentence
    Summary · context
    IUGR was induced by bilateral uterine artery ligation in fetal life. Ex-4 was given on postnatal days 1-6 of life. Islets were isolated at 1 week and at 3-12 months.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In IUGR rat islets, exendin‑4 permanently increased H3K4 trimethylation at the Pdx1 promoter.

    In plain wordsIn rats with restricted fetal growth, exendin‑4 permanently increased H3K4 trimethylation at the Pdx1 promoter.

    Outcome
    IncreaseH3K4 trimethylation
    Study

    ratn: not reported in source

    Intrauterine growth retardation
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated · postnatal days 1-6As given in this study (rat).

    Source sentences

    Summary
    Histone H3 acetylation and trimethylation of H3K4 were permanently increased, whereas Dnmt1 binding and subsequent DNA methylation were prevented at the proximal promoter of Pdx1 in IUGR islets.
    1 context sentence
    Summary · context
    IUGR was induced by bilateral uterine artery ligation in fetal life. Ex-4 was given on postnatal days 1-6 of life. Islets were isolated at 1 week and at 3-12 months.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In IUGR rat islets, exendin‑4 prevented Dnmt1 binding at the Pdx1 promoter.

    In plain wordsIn rats with restricted fetal growth, exendin‑4 prevented Dnmt1 binding at the Pdx1 promoter.

    Outcome
    DecreaseDnmt1 binding
    Study

    ratn: not reported in source

    Intrauterine growth retardation
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated · postnatal days 1-6As given in this study (rat).

    Source sentences

    Summary
    Histone H3 acetylation and trimethylation of H3K4 were permanently increased, whereas Dnmt1 binding and subsequent DNA methylation were prevented at the proximal promoter of Pdx1 in IUGR islets.
    1 context sentence
    Summary · context
    IUGR was induced by bilateral uterine artery ligation in fetal life. Ex-4 was given on postnatal days 1-6 of life. Islets were isolated at 1 week and at 3-12 months.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In IUGR rat islets, exendin‑4 prevented DNA methylation at the Pdx1 promoter.

    In plain wordsIn rats with restricted fetal growth, exendin‑4 prevented DNA methylation at the Pdx1 promoter.

    Outcome
    DecreasePdx1 promoter DNA methylation
    Study

    ratn: not reported in source

    Intrauterine growth retardation
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated · postnatal days 1-6As given in this study (rat).

    Source sentences

    Summary
    Histone H3 acetylation and trimethylation of H3K4 were permanently increased, whereas Dnmt1 binding and subsequent DNA methylation were prevented at the proximal promoter of Pdx1 in IUGR islets.
    1 context sentence
    Summary · context
    IUGR was induced by bilateral uterine artery ligation in fetal life. Ex-4 was given on postnatal days 1-6 of life. Islets were isolated at 1 week and at 3-12 months.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In IUGR rat islets, normalization of epigenetic modifications after exendin‑4 reversed Pdx1 silencing.

    In plain wordsIn rats with restricted fetal growth, epigenetic changes after exendin‑4 reversed Pdx1 silencing.

    Outcome
    DecreasePdx1 silencing
    Study

    ratn: not reported in source

    Intrauterine growth retardation
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated · postnatal days 1-6As given in this study (rat).

    Source sentences

    Summary
    Normalisation of these epigenetic modifications reversed silencing of Pdx1 in islets of IUGR animals.
    2 context sentences
    Summary · context
    Histone H3 acetylation and trimethylation of H3K4 were permanently increased, whereas Dnmt1 binding and subsequent DNA methylation were prevented at the proximal promoter of Pdx1 in IUGR islets.
    Summary · context
    IUGR was induced by bilateral uterine artery ligation in fetal life. Ex-4 was given on postnatal days 1-6 of life. Islets were isolated at 1 week and at 3-12 months.

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

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