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Study · Measured the body's own peptide · 2009

2 results

The mammalian target of rapamycin as novel central regulator of puberty onset via modulation of hypothalamic Kiss1 system.

Roa J, Garcia-Galiano D, Varela L, Sánchez-Garrido MA, Pineda R, Castellano JM, Ruiz-Pino F, Romero M, Aguilar E, López M, Gaytan F, Diéguez C, Pinilla L, Tena-Sempere M

Endocrinology4 Sept 2009Cited by 186 (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 study2

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

Natural levels measured1

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)Mechanism

    In female rats, inactivation of central mTOR decreased hypothalamic Kiss1 expression, with a dramatic fall in Kiss1 mRNA at the arcuate nucleus.

    In plain wordsIn rats, blocking mTOR lowered the body's own Kiss1 (the gene for kisspeptin) activity in the brain.

    Outcome
    DecreaseHypothalamic Kiss1 expression after mTOR inactivation
    Study

    ratn: not reported in source

    Outcome group
    Sex hormones and fertility · Endocrine and hormones

    Source sentences

    Summary
    Finally, mTOR inactivation evoked a significant decrease of Kiss1 expression at the hypothalamus, with dramatic suppression of Kiss1 mRNA levels at the arcuate nucleus.
    1 context sentence
    Summary · context
    Conversely, blockade of central mTOR signaling by rapamycin caused inhibition of the gonadotropic axis at puberty, with significantly delayed vaginal opening, decreased LH and estradiol levels, and ovarian and uterine atrophy.

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

Studies that did not test the peptide alone1

In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Kisspeptin-10.

  1. 02AnimalNot a test of Kisspeptin-10 aloneAnimal study (in vivo)Efficacy outcome

    In female rats with sustained central mTOR blockade by rapamycin, the GnRH/LH system still responded to kisspeptin‑10, so rapamycin did not disrupt GnRH function.

    In plain wordsIn rats, the hormone system still responded to kisspeptin‑10 after mTOR was blocked, so the block did not damage it.

    Outcome
    No significant changeLH response to kisspeptin-10 after mTOR blockade
    Study

    ratn: not reported in source

    Outcome group
    Sex hormones and fertility · Endocrine and hormones

    Source sentences

    Summary
    Yet the GnRH/LH system retained their ability to respond to ovariectomy and kisspeptin-10 after sustained blockade of mTOR, ruling out the possibility of unspecific disruption of GnRH function by rapamycin.
    1 context sentence
    Summary · context
    Conversely, blockade of central mTOR signaling by rapamycin caused inhibition of the gonadotropic axis at puberty, with significantly delayed vaginal opening, decreased LH and estradiol levels, and ovarian and uterine atrophy.

    In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.

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

    10 Oct 2026, 09:43 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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