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Study · Not a test of the peptide alone · 2013

1 result

Pituitary phenotypes of mice lacking the notch signalling ligand delta-like 1 homologue.

Cheung LY, Rizzoti K, Lovell-Badge R, Le Tissier PR

Journal of neuroendocrinology1 Apr 2013Cited by 35 (Europe PMC)

PMID23279263 (opens in a new tab)PMCIDPMC3664429 (opens in a new tab)DOI10.1111/jne.12010 (opens in a new tab)PepBankPUB-23279263
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Summary

The Notch signalling pathway ligand delta-like 1 homologue (Dlk1, also named Pref1) is expressed throughout the developing pituitary and becomes restricted to mostly growth hormone (GH) cells within the adult gland. We have investigated the role of Dlk1 in pituitary development and function from late embryogenesis to adulthood using a mouse model completely lacking the expression of Dlk1. We confirm that Dlk1-null mice are shorter and weigh less than wild-type littermates from late gestation, at parturition and in adulthood. A loss of Dlk1 leads to significant reduction in GH content throughout life, whereas other pituitary hormones are reduced to varying degrees depending on sex and age. Both the size of the pituitary and the proportion of hormone-producing cell populations are unchanged, suggesting that there is a reduction in hormone content per cell. In vivo challenge of mutant and wild-type littermates with growth hormone-releasing hormone and growth hormone-releasing hexapeptide shows that reduced GH secretion is unlikely to account for the reduced growth of Dlk1 knockout animals. These data suggest that loss of Dlk1 gives rise to minor pituitary defects manifesting as an age- and sex-dependent reduction in pituitary hormone contents. However, Dlk1 expression in other tissue is most likely responsible for the weight and length differences observed in mutant animals.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

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

Studies that did not test the peptide alone1

In this study, GHRP-6 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 GHRP-6.

  1. 01AnimalNot a test of GHRP-6 aloneAnimal study (in vivo)Mechanism

    In Dlk1-null and wild-type mice, GHRH and growth hormone-releasing hexapeptide challenges suggested reduced GH secretion was unlikely to explain reduced knockout growth.

    In plain wordsIn mice, hormone challenges suggested reduced growth hormone secretion was unlikely to explain reduced growth of Dlk1-null animals.

    Peptide
    GHRP-6
    Outcome
    Direction not reportedGrowth hormone secretion after challenge
    Study

    mousen: not reported in source

    Dlk1-null mice and wild-type littermates
    Outcome group
    Growth hormone and IGF-1 · Endocrine and hormones

    Source sentences

    Summary
    In vivo challenge of mutant and wild-type littermates with growth hormone-releasing hormone and growth hormone-releasing hexapeptide shows that reduced GH secretion is unlikely to account for the reduced growth of Dlk1 knockout animals.

    In this study, GHRP-6 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 GHRP-6.

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

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:13 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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