Evidence mapPaperPMID 23169784Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2013

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

Kikuo Yo, Yong-Ming Yu, Gaofeng Zhao, Ali A Bonab, Naoki Aikawa, Ronald G Tompkins, Alan J Fischman

Abstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Observational
  3. Article
  4. Article
  5. Brown adipose tissue recruitment in a rodent model of severe burns.Burns : journal of the International Society for Burn Injuries · 2020
    Article
  6. Adipose Tissue Metabolic Function and Dysfunction: Impact of Burn Injury.Frontiers in cell and developmental biology · 2020
    Review
  7. Article
  8. Article
  9. Review
  10. Differential acute and chronic effects of burn trauma on murine skeletal muscle bioenergetics.Burns : journal of the International Society for Burn Injuries · 2016
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Kikuo YoShriners Hospitals for Children, Boston, 51 Blossom St., Boston, MA 02114, USA. aajjff@gmail.com
Yong-Ming Yu
Gaofeng Zhao
Ali A Bonab
Naoki Aikawa
Ronald G Tompkins
Alan J Fischman
Massachusetts General Hospital · USHarvard University · USKeio University · JPShriners Hospitals for Children - Boston · US

Funding

WOUND HEALINGP50GM021700 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI TOMPKINS, RONALD GARY · 1985 to 2017
$27.2M
TRAINING IN BURNS AND TRAUMA RESEARCHT32GM007035 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI TOMPKINS, RONALD GARY · 1985 to 2014
$3.5M
NIDDK NIH HHS P30 DK-004056NIGMS NIH HHS 2P50 GM-21700-27ANIGMS NIH HHS P50 GM021700NIGMS NIH HHS T32 GM007035
6 · The paper itself

Abstract

Hypermetabolism is a prominent feature of burn injury, and altered mitochondria function is presumed to contribute to this state. Recently, brown adipose tissue (BAT) was found to be present not only in rodents but also in humans, and its activity is associated with resting metabolic rate. 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. We demonstrate that burn injury induces morphological changes in interscapular BAT (iBAT). Burn injury was associated with iBAT activation, and this effect was positively correlated with increased energy expenditure. BAT activation was associated with augmentation of mitochondria biogenesis, and UCP1 expression in the isolated iBAT mitochondria. In addition, the mitochondria-targeted peptide SS31 attenuated burn injury-induced hypermetabolism, which was accompanied by suppression of UCP1 expression in isolated mitochondria. Our results suggest that BAT plays an important role in burn injury-induced hypermetabolism through its morphological changes and expression of UCP1.

Indexed as

Adipose Tissue, BrownAnimalsBurnsDown-RegulationEnergy MetabolismFree Radical ScavengersIon ChannelsMaleMicroscopy, Electron, TransmissionMitochondriaMitochondrial DiseasesMitochondrial ProteinsMitochondrial TurnoverMolecular Targeted TherapyOligopeptidesRandom Allocationarginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamideFree Radical ScavengersIon ChannelsMitochondrial ProteinsOligopeptidesUCP1 protein, humanUcp1 protein, ratUncoupling Protein 1

Identifiers

PMID23169784
PMCPMC3566510
OpenAlexW2091057486

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.