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Study · Not a test of the peptide alone · 2022

2 results

Enteral nutrition alleviated lipopolysaccharides-induced hypercatabolism through ghrelin/GHS-R1α-POMC.

Cao C, Zhang Y, Zuo S, Zhao W, Wu Y, Ma X

Biochemical and biophysical research communications2 Feb 2022Cited by 5 (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.

Studies that did not test the peptide alone2

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 endotoxemic rats, central D-Lys3-GHRP‑6 abolished the improvement in hypercatabolism from enteral nutrition.

    In plain wordsIn endotoxemic rats, D-Lys3-GHRP‑6 abolished the improvement in hypercatabolism compared with enteral nutrition alone.

    Peptide
    GHRP-6
    Outcome
    Direction not reportedHypercatabolism response to enteral nutrition
    Study

    ratn: not reported in source

    Endotoxemic rats
    Comparator
    Enteral nutrition without antagonist
    Outcome group
    Metabolic pathways and metabolomics · Metabolic and weight

    Source sentences

    Summary
    The improving effects of EN on hypercatabolism and hypothalamic AMPK-autophagy-POMC pathway were abolished with the central administration of D-Lys3-GHRP-6 to inhibited hypothalamic GHS-R1α.
    2 context sentences
    Summary · context
    Therefore, we tested whether EN alleviated hypercatabolism through ghrelin/GH secretagogue receptor 1α (GHS-R1α)-proopiomelanocortin (POMC) in endotoxemic rats.
    Summary · context
    Rats in the EN, EN + Lys and EN + 3-MA groups were intracerebroventricularly injected with saline, D-Lys3-GHRP-6 or 3-MA and then received EN for three days.

    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.

  2. 02AnimalNot a test of GHRP-6 aloneAnimal study (in vivo)Mechanism

    In endotoxemic rats, central D-Lys3-GHRP‑6 abolished the effect of enteral nutrition on the hypothalamic AMPK-autophagy-POMC pathway.

    In plain wordsIn endotoxemic rats, D-Lys3-GHRP‑6 abolished hypothalamic pathway activation compared with enteral nutrition alone.

    Peptide
    GHRP-6
    Outcome
    DecreaseHypothalamic AMPK-autophagy-POMC pathway response
    Study

    ratn: not reported in source

    Endotoxemic rats
    Comparator
    Enteral nutrition without antagonist
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition

    Source sentences

    Summary
    The improving effects of EN on hypercatabolism and hypothalamic AMPK-autophagy-POMC pathway were abolished with the central administration of D-Lys3-GHRP-6 to inhibited hypothalamic GHS-R1α.
    2 context sentences
    Summary · context
    Therefore, we tested whether EN alleviated hypercatabolism through ghrelin/GH secretagogue receptor 1α (GHS-R1α)-proopiomelanocortin (POMC) in endotoxemic rats.
    Summary · context
    Rats in the EN, EN + Lys and EN + 3-MA groups were intracerebroventricularly injected with saline, D-Lys3-GHRP-6 or 3-MA and then received EN for three days.

    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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