Skip to content

Study · Animal study (in vivo) · mouse · 2021

8 results

MOTS-c reduces myostatin and muscle atrophy signaling.

Kumagai H, Coelho AR, Wan J, Mehta HH, Yen K, Huang A, Zempo H, Fuku N, Maeda S, Oliveira PJ, Cohen P, Kim SJ

American journal of physiology. Endocrinology and metabolism8 Feb 2021Cited by 56 (Europe PMC)

PMID33554779 (opens in a new tab)PMCIDPMC8238132 (opens in a new tab)DOI10.1152/ajpendo.00275.2020 (opens in a new tab)PepBankPUB-33554779
Source linkPubMedAsk about this study
Jump to 8 results

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 study8

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In diet-induced obese mice, MOTS‑c administration decreased myostatin levels in plasma.

    In plain wordsIn obese mice, MOTS‑c lowered myostatin, a muscle-wasting signal, in blood.

    Peptide
    MOTS-c
    Outcome
    DecreasePlasma myostatin in obese mice
    Study

    mousen: not reported in source

    Diet-induced obese mice
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    whereas MOTS-c administration decreased myostatin levels in plasma in diet-induced obese mice.
  2. 02LabIn vitro (cells)Efficacy outcome

    In differentiated C2C12 myotubes, MOTS‑c prevented palmitic acid-induced atrophy.

    In plain wordsIn cells, MOTS‑c prevented muscle cell shrinking caused by palmitic acid.

    Peptide
    MOTS-c
    Outcome
    DecreasePalmitic acid-induced atrophy in C2C12 myotubes
    Study

    n: not reported in source

    Differentiated C2C12 myotubes
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We further demonstrated that MOTS-c prevents palmitic acid-induced atrophy in differentiated C2C12 myotubes
  3. 03LabIn vitro (cells)Mechanism

    In the cell model, MOTS‑c elevated AKT phosphorylation.

    In plain wordsIn cells, MOTS‑c increased AKT phosphorylation, a growth signal.

    Peptide
    MOTS-c
    Outcome
    IncreaseAKT phosphorylation
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    By elevating AKT phosphorylation, MOTS-c inhibits the activity of an upstream transcription factor for myostatin and other muscle wasting genes, FOXO1.
  4. 04LabIn vitro (cells)Mechanism

    In the cell model, MOTS‑c inhibited the activity of FOXO1, a transcription factor for myostatin and other muscle wasting genes.

    In plain wordsIn cells, MOTS‑c reduced the activity of FOXO1, which switches on muscle-wasting genes.

    Peptide
    MOTS-c
    Outcome
    DecreaseFOXO1 activity
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    By elevating AKT phosphorylation, MOTS-c inhibits the activity of an upstream transcription factor for myostatin and other muscle wasting genes, FOXO1.
  5. 05LabIn vitro (cells)Mechanism

    In the cell model, MOTS‑c increased mTORC2.

    In plain wordsIn cells, MOTS‑c increased the activity of mTORC2, a growth-signal protein.

    Peptide
    MOTS-c
    Outcome
    IncreasemTORC2 activity
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    MOTS-c increases mTORC2 and inhibits PTEN activity, which modulates AKT phosphorylation.
  6. 06LabIn vitro (cells)Mechanism

    In the cell model, MOTS‑c inhibited PTEN activity.

    In plain wordsIn cells, MOTS‑c reduced the activity of PTEN, a protein that limits AKT.

    Peptide
    MOTS-c
    Outcome
    DecreasePTEN activity
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    MOTS-c increases mTORC2 and inhibits PTEN activity, which modulates AKT phosphorylation.
  7. 07LabIn vitro (cells)Mechanism

    In the cell model, MOTS‑c increased CK2 activity, which leads to PTEN inhibition.

    In plain wordsIn cells, MOTS‑c increased CK2 activity, which in turn lowers PTEN activity.

    Peptide
    MOTS-c
    Outcome
    IncreaseCK2 activity
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Further upstream, MOTS-c increases CK2 activity, which leads to PTEN inhibition.

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. 08HumanEndogenous levelObservational studyOther

    In human subjects, plasma MOTS‑c levels were inversely correlated with myostatin levels.

    In plain wordsIn people, higher natural MOTS‑c levels in blood were linked to lower myostatin levels.

    Peptide
    MOTS-c
    Outcome
    Not applicableAssociation of plasma MOTS-c with myostatin in humans
    Study

    n: not reported in source

    Outcome group
    Muscle injury and repair · Musculoskeletal

    Source sentences

    Summary
    Interestingly, we found that plasma MOTS-c levels are inversely correlated with myostatin levels in human subjects.

    This result measures the body's own MOTS-c. 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, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.