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Study · Animal study (in vivo) · rat · 2013

2 results

Brown adipose tissue and its modulation by a mitochondria-targeted peptide in rat burn injury-induced hypermetabolism.

Yo K, Yu YM, Zhao G, Bonab AA, Aikawa N, Tompkins RG, Fischman AJ

American journal of physiology. Endocrinology and metabolism20 Nov 2012Cited by 26 (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

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In rats with burn injury, the mitochondria-targeted peptide SS31 attenuated burn injury-induced hypermetabolism.

    In plain wordsIn rats with burn injury, SS31 reduced the raised metabolic rate that burns cause.

    Outcome
    DecreaseBurn injury-induced hypermetabolism
    Study

    ratn: not reported in source

    Rat burn injury-induced hypermetabolism
    Comparator
    Burn injury without SS31
    Outcome group
    Energy expenditure and thermogenesis · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, the mitochondria-targeted peptide SS31 attenuated burn injury-induced hypermetabolism, which was accompanied by suppression of UCP1 expression in isolated mitochondria.
    1 context sentence
    Summary · context
    In this report, we elucidate the relationship between burn injury-induced hypermetabolism and BAT activity and the possible role of the mitochondria-targeted peptide SS31 in attenuating burn injury-induced hypermetabolism by using a rat burn injury model.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In rats with burn injury, SS31 was accompanied by suppression of UCP1 expression in isolated brown adipose tissue mitochondria.

    In plain wordsIn rats with burn injury, SS31 treatment came with lower UCP1, a heat-producing protein, in brown fat mitochondria.

    Outcome
    DecreaseUCP1 expression in isolated brown fat mitochondria
    Study

    ratn: not reported in source

    Rat burn injury-induced hypermetabolism
    Comparator
    Burn injury without SS31
    Outcome group
    Mitochondrial function · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, the mitochondria-targeted peptide SS31 attenuated burn injury-induced hypermetabolism, which was accompanied by suppression of UCP1 expression in isolated mitochondria.
    1 context sentence
    Summary · context
    In this report, we elucidate the relationship between burn injury-induced hypermetabolism and BAT activity and the possible role of the mitochondria-targeted peptide SS31 in attenuating burn injury-induced hypermetabolism by using a rat burn injury model.

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

    10 Oct 2026, 08:19 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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