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Study · Measured the body's own peptide · 2008

2 results

Absence of gonadotropin-releasing hormone 1 and Kiss1 activation in alpha-fetoprotein knockout mice: prenatal estrogens defeminize the potential to show preovulatory luteinizing hormone surges.

González-Martínez D, De Mees C, Douhard Q, Szpirer C, Bakker J

Endocrinology17 Jan 2008Cited by 50 (Europe PMC)

PMID18202134 (opens in a new tab)PMCIDPMC2329285 (opens in a new tab)DOI10.1210/en.2007-1422 (opens in a new tab)PepBankPUB-18202134
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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 study2

No result from this study comes from a test of the peptide.

Natural levels measured2

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 01AnimalEndogenous levelAnimal study (in vivo)Other

    In alpha-fetoprotein knockout female mice, kisspeptin‑10 immunoreactivity was lower.

    In plain wordsIn mice lacking alpha-fetoprotein, females had less of the body's own kisspeptin‑10 signal in the brain.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseKisspeptin-10 immunoreactivity in Afp(-/-) females
    Study

    mousen: not reported in source

    alpha-fetoprotein knockout mice (Afp-/-)
    Outcome group
    Endogenous peptide levels · Endocrine and hormones

    Source sentences

    Summary
    Furthermore, Kisspeptin-10 immunoreactivity and neural activation, measured by the number of double-labeled FOS/Kisspeptin-10 cells, were lower in Afp(-/-) females, suggesting a down-regulation of GnRH1 function.
    1 context sentence
    Summary · context
    Because the KISS1/GPR54 system is a key upstream regulator of the GnRH1 system as well as being sexually dimorphic, we also analyzed whether Kisspeptin-10 neurons were activated in Afp(-/-) mice after treatment with estradiol and progesterone.

    This result measures the body's own Kisspeptin-10. Nobody was given the peptide. It is not evidence about taking it.

  2. 02AnimalEndogenous levelAnimal study (in vivo)Other

    In alpha-fetoprotein knockout female mice given estradiol and progesterone, fewer kisspeptin‑10 neurons were activated, as shown by FOS double labeling.

    In plain wordsIn mice lacking alpha-fetoprotein, fewer of the body's own kisspeptin‑10 neurons were switched on after hormone treatment.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseFOS/Kisspeptin-10 double-labeled neuron count in Afp(-/-) females
    Study

    mousen: not reported in source

    alpha-fetoprotein knockout mice (Afp-/-)
    Outcome group
    Endogenous peptide levels · Endocrine and hormones

    Source sentences

    Summary
    Furthermore, Kisspeptin-10 immunoreactivity and neural activation, measured by the number of double-labeled FOS/Kisspeptin-10 cells, were lower in Afp(-/-) females, suggesting a down-regulation of GnRH1 function.
    1 context sentence
    Summary · context
    Because the KISS1/GPR54 system is a key upstream regulator of the GnRH1 system as well as being sexually dimorphic, we also analyzed whether Kisspeptin-10 neurons were activated in Afp(-/-) mice after treatment with estradiol and progesterone.

    This result measures the body's own Kisspeptin-10. Nobody was given the peptide. It is not evidence about taking it.

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

    9 Oct 2026, 18:17 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:04 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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