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Study · Animal study (in vivo) · mouse · 2015

6 results

The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance.

Lee C, Zeng J, Drew BG, Sallam T, Martin-Montalvo A, Wan J, Kim SJ, Mehta H, Hevener AL, de Cabo R, de Cabo R, Cohen P

Cell metabolism1 Mar 2015Cited by 584 (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 study6

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice, MOTS‑c treatment prevented age-dependent insulin resistance.

    In plain wordsIn mice, MOTS‑c treatment prevented insulin resistance that comes with age.

    Peptide
    MOTS-c
    Outcome
    DecreaseAge-dependent insulin resistance
    Study

    mousen: not reported in source

    Aged mice
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    MOTS-c treatment in mice prevented age-dependent and high-fat-diet-induced insulin resistance, as well as diet-induced obesity.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice, MOTS‑c treatment prevented high-fat-diet-induced insulin resistance.

    In plain wordsIn mice, MOTS‑c treatment prevented insulin resistance caused by a high-fat diet.

    Peptide
    MOTS-c
    Outcome
    DecreaseHigh-fat-diet-induced insulin resistance
    Study

    mousen: not reported in source

    High-fat-diet mice
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    MOTS-c treatment in mice prevented age-dependent and high-fat-diet-induced insulin resistance, as well as diet-induced obesity.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice, MOTS‑c treatment prevented diet-induced obesity.

    In plain wordsIn mice, MOTS‑c treatment prevented weight gain from a high-fat diet.

    Peptide
    MOTS-c
    Outcome
    DecreaseDiet-induced obesity
    Study

    mousen: not reported in source

    High-fat-diet mice
    Outcome group
    Body weight · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    MOTS-c treatment in mice prevented age-dependent and high-fat-diet-induced insulin resistance, as well as diet-induced obesity.
  4. 04LabIn vitro (cells)Mechanism

    In cells, MOTS‑c actions inhibited the folate cycle.

    In plain wordsIn cells, MOTS‑c reduced the activity of the folate cycle.

    Peptide
    MOTS-c
    Outcome
    DecreaseFolate cycle activity
    Study

    n: not reported in source

    Cells
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Its primary target organ appears to be the skeletal muscle, and its cellular actions inhibit the folate cycle and its tethered de novo purine biosynthesis, leading to AMPK activation.
  5. 05LabIn vitro (cells)Mechanism

    In cells, MOTS‑c actions inhibited de novo purine biosynthesis tethered to the folate cycle.

    In plain wordsIn cells, MOTS‑c reduced the making of purines, building blocks of DNA.

    Peptide
    MOTS-c
    Outcome
    DecreaseDe novo purine biosynthesis
    Study

    n: not reported in source

    Cells
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Its primary target organ appears to be the skeletal muscle, and its cellular actions inhibit the folate cycle and its tethered de novo purine biosynthesis, leading to AMPK activation.
  6. 06LabIn vitro (cells)Mechanism

    In cells, MOTS‑c actions led to AMPK activation.

    In plain wordsIn cells, MOTS‑c switched on the enzyme AMPK.

    Peptide
    MOTS-c
    Outcome
    IncreaseAMPK activation
    Study

    n: not reported in source

    Cells
    Outcome group
    Receptor activity and mechanism · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Its primary target organ appears to be the skeletal muscle, and its cellular actions inhibit the folate cycle and its tethered de novo purine biosynthesis, leading to AMPK activation.

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. Versions 4 to 18Current

    28 Oct 2026, 02:02 UTC

    The same notice was added 15 times, first on 13 Oct 2026, 21:44 UTC. The status did not change between them.

    Study results updated

  2. Version 3

    13 Oct 2026, 16:31 UTC

    Study data updated · source update from Europe PMC

  3. Version 2

    9 Oct 2026, 18:17 UTC

    Study results updated

  4. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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