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Study · Animal study (in vivo) · 2019

6 results

Mitochondrial-Derived Peptide MOTS-c Increases Adipose Thermogenic Activation to Promote Cold Adaptation.

Lu H, Tang S, Xue C, Liu Y, Wang J, Zhang W, Luo W, Chen J

International journal of molecular sciences17 May 2019Cited by 53 (Europe PMC)

PMID31109005 (opens in a new tab)PMCIDPMC6567243 (opens in a new tab)DOI10.3390/ijms20102456 (opens in a new tab)PepBankPUB-31109005
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Summary

Cold exposure stress causes hypothermia, cognitive impairment, liver injury, and cardiovascular diseases, thereby increasing morbidity and mortality. Paradoxically, cold acclimation is believed to confer metabolic improvement to allow individuals to adapt to cold, harsh conditions and to protect them from cold stress-induced diseases. However, the therapeutic strategy to enhance cold acclimation remains less studied. Here, we demonstrate that the mitochondrial-derived peptide MOTS-c efficiently promotes cold adaptation. Following cold exposure, the improvement of adipose non-shivering thermogenesis facilitated cold adaptation. MOTS-c, a newly identified peptide, is secreted by mitochondria. In this study, we observed that the level of MOTS-c in serum decreased after cold stress. MOTS-c treatment enhanced cold tolerance and reduced lipid trafficking to the liver. In addition, MOTS-c dramatically upregulated brown adipose tissue (BAT) thermogenic gene expression and increased white fat "browning". This effect might have been mediated by MOTS-c-activated phosphorylation of the ERK signaling pathway. The inhibition of ERK signaling disturbed the up-regulatory effect of MOTS-c on thermogenesis. In summary, our results indicate that MOTS-c treatment is a potential therapeutic strategy for defending against cold stress by increasing the adipose thermogenesis via the ERK pathway.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study6

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In cold-exposed animals, MOTS‑c treatment enhanced cold tolerance.

    In plain wordsIn animals, MOTS‑c treatment improved tolerance to cold.

    Peptide
    MOTS-c
    Outcome
    IncreaseCold tolerance
    Study

    n: not reported in source

    Outcome group
    Body temperature · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    MOTS-c treatment enhanced cold tolerance and reduced lipid trafficking to the liver.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In cold-exposed animals, MOTS‑c treatment reduced lipid trafficking to the liver.

    In plain wordsIn animals in the cold, MOTS‑c treatment reduced the movement of fat to the liver.

    Peptide
    MOTS-c
    Outcome
    DecreaseLipid trafficking to the liver
    Study

    n: not reported in source

    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    MOTS-c treatment enhanced cold tolerance and reduced lipid trafficking to the liver.
  3. 03AnimalAnimal study (in vivo)Mechanism

    MOTS‑c dramatically upregulated brown adipose tissue thermogenic gene expression.

    In plain wordsIn animals, MOTS‑c turned up genes for heat production in brown fat.

    Peptide
    MOTS-c
    Outcome
    IncreaseBAT thermogenic gene expression
    Study

    n: not reported in source

    Outcome group
    Mitochondrial function · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, MOTS-c dramatically upregulated brown adipose tissue (BAT) thermogenic gene expression and increased white fat "browning".
  4. 04AnimalAnimal study (in vivo)Mechanism

    MOTS‑c increased white fat browning.

    In plain wordsIn animals, MOTS‑c increased the change of white fat toward heat-producing brown-like fat.

    Peptide
    MOTS-c
    Outcome
    IncreaseWhite fat browning
    Study

    n: not reported in source

    Outcome group
    Mitochondrial function · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, MOTS-c dramatically upregulated brown adipose tissue (BAT) thermogenic gene expression and increased white fat "browning".
  5. 05AnimalAnimal study (in vivo)Mechanism

    Inhibition of ERK signaling disturbed the up-regulatory effect of MOTS‑c on thermogenesis.

    In plain wordsIn animals, blocking ERK signaling weakened the heat-production effect of MOTS‑c.

    Peptide
    MOTS-c
    Outcome
    Not applicableThermogenesis effect after ERK inhibition
    Study

    n: not reported in source

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

    Source sentences

    Summary
    The inhibition of ERK signaling disturbed the up-regulatory effect of MOTS-c on thermogenesis.

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. 06AnimalEndogenous levelAnimal study (in vivo)Other

    In cold-stressed animals, serum MOTS‑c levels decreased after cold stress.

    In plain wordsIn animals, the body's own MOTS‑c in the blood fell after cold stress.

    Peptide
    MOTS-c
    Outcome
    DecreaseSerum MOTS-c level after cold stress
    Study

    n: not reported in source

    Outcome group
    Mitochondrial function · Metabolic and weight

    Source sentences

    Summary
    In this study, we observed that the level of MOTS-c in serum decreased after cold stress.

    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.

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