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Study · Animal study (in vivo) · mouse · 2007

4 results

Central melanocortin signaling restores skeletal muscle AMP-activated protein kinase phosphorylation in mice fed a high-fat diet.

Tanaka T, Masuzaki H, Yasue S, Ebihara K, Shiuchi T, Ishii T, Arai N, Hirata M, Yamamoto H, Hayashi T, Hosoda K, Minokoshi Y, Nakao K

Cell metabolism1 May 2007Cited by 48 (Europe PMC)

PMID17488641 (opens in a new tab)DOI10.1016/j.cmet.2007.04.004 (opens in a new tab)PepBankPUB-17488641
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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 study4

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In mice, central MT-II increased skeletal muscle AMPK phosphorylation independent of caloric intake.

    In plain wordsIn mice, Melanotan II given into the brain raised a muscle energy-signaling marker, regardless of how much the mice ate.

    Peptide
    Melanotan II
    Outcome
    IncreaseSkeletal muscle AMPK phosphorylation
    Study

    mousen: not reported in source

    Conscious, unrestrained mice
    Outcome group
    Metabolic pathways and metabolomics · Metabolic and weight
    Studied dose
    Dose not stated · intracerebroventricularAs given in this study (mouse).

    Source sentences

    Summary
    MT-II augmented phosphorylation of AMPK and its target acetyl-CoA carboxylase (ACC) independent of caloric intake.
    1 context sentence
    Summary · context
    To elucidate an unidentified role of the central melanocortin system in muscle AMPK regulation, we treated conscious, unrestrained mice intracerebroventricularly with the melanocortin agonist MT-II or the antagonist SHU9119.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mice, central MT-II increased skeletal muscle phosphorylation of the AMPK target ACC independent of caloric intake.

    In plain wordsIn mice, Melanotan II given into the brain raised a second muscle energy-signaling marker, regardless of how much the mice ate.

    Peptide
    Melanotan II
    Outcome
    IncreaseSkeletal muscle ACC phosphorylation
    Study

    mousen: not reported in source

    Conscious, unrestrained mice
    Outcome group
    Metabolic pathways and metabolomics · Metabolic and weight
    Studied dose
    Dose not stated · intracerebroventricularAs given in this study (mouse).

    Source sentences

    Summary
    MT-II augmented phosphorylation of AMPK and its target acetyl-CoA carboxylase (ACC) independent of caloric intake.
    1 context sentence
    Summary · context
    To elucidate an unidentified role of the central melanocortin system in muscle AMPK regulation, we treated conscious, unrestrained mice intracerebroventricularly with the melanocortin agonist MT-II or the antagonist SHU9119.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In leptin-overexpressing transgenic mice on a high-fat diet, MT-II markedly restored the attenuated AMPK phosphorylation, which central leptin did not reverse.

    In plain wordsIn mice on a high-fat diet, Melanotan II restored a muscle energy-signaling marker that had fallen.

    Peptide
    Melanotan II
    Outcome
    IncreaseAMPK phosphorylation in high-fat-diet leptin-overexpressing mice
    Study

    mousen: not reported in source

    Leptin-overexpressing transgenic mice fed a high-fat diet
    Outcome group
    Metabolic pathways and metabolomics · Metabolic and weight
    Studied dose
    Dose not stated · intracerebroventricularAs given in this study (mouse).

    Source sentences

    Summary
    Importantly, high-fat-diet-induced attenuation of AMPK/ACC phosphorylation in leptin-overexpressing transgenic mice was not reversed by central leptin but was markedly restored by MT-II.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In leptin-overexpressing transgenic mice on a high-fat diet, MT-II markedly restored the attenuated ACC phosphorylation, which central leptin did not reverse.

    In plain wordsIn mice on a high-fat diet, Melanotan II restored a second muscle energy-signaling marker that had fallen.

    Peptide
    Melanotan II
    Outcome
    IncreaseACC phosphorylation in high-fat-diet leptin-overexpressing mice
    Study

    mousen: not reported in source

    Leptin-overexpressing transgenic mice fed a high-fat diet
    Outcome group
    Metabolic pathways and metabolomics · Metabolic and weight
    Studied dose
    Dose not stated · intracerebroventricularAs given in this study (mouse).

    Source sentences

    Summary
    Importantly, high-fat-diet-induced attenuation of AMPK/ACC phosphorylation in leptin-overexpressing transgenic mice was not reversed by central leptin but was markedly restored by MT-II.

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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