Evidence map›Paper›PMID 26586436›Full record

ArticleCell reports2015

Burn Induces Browning of the Subcutaneous White Adipose Tissue in Mice and Humans.

David Patsouris, Peter Qi, Abdikarim Abdullahi, Mile Stanojcic, Peter Chen, Alexandra Parousis, Saeid Amini-Nik, Marc G Jeschke

Registry-linked trialAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06899958 (Metabolism Enhancement by Laser Therapy), which is not on this map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
–field-weighted citation impact
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.

NCT06899958 nanot yet recruitingnot on this mapstarted 2027, after this paper: background citation

Metabolism Enhancement by Laser Therapy

TypeinterventionalSponsorMassachusetts General HospitalRan2027 to 2029Enrolled15ConditionsMetabolism DisorderArmsFractional Laser
3 · Its place in the literature

Who cites it

117 citing papers in PubMed.

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57 more citing papers are in PubMed but not listed here.

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

8 authors.

David PatsourisDepartment of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada.
Peter QiDepartment of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada.
Abdikarim AbdullahiDepartment of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada.
Mile StanojcicDepartment of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada.
Peter ChenDepartment of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada.
Alexandra ParousisDepartment of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada.
Saeid Amini-NikSunnybrook Research Institute, Toronto, ON M4N 3M5, Canada; Department of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada.
Marc G JeschkeRoss Tilley Burn Centre, Sunnybrook Health Sciences Centre, Sunnybrook Research Institute, Toronto, ON M4N 3M5, Canada; Sunnybrook Research Institute, Toronto, ON M4N 3M5, Canada; Department of Surgery, Division of Plastic Surgery, Department of Immunology, University of Toronto, Toronto, ON M5S 1A1, Canada. Electronic address: marc.jeschke@sunnybrook.ca.

Funding

Hepatic ER stress contributes to morbidity and mortality after burn injury.R01GM087285 · NIGMS · SUNNYBROOK & WOMEN'S COLL HLTH SCIS CTR · PI BOEHNING, DARREN F, JESCHKE, MARC GERHARD · 2010 to 2018
$1.9M
Canadian Institutes of Health Research 123336NIGMS NIH HHS NIH 2R01GM087285-05A1NIGMS NIH HHS R01 GM087285
6 · The paper itself

Abstract

Burn is accompanied by long-lasting immuno-metabolic alterations referred to as hypermetabolism that are characterized by a considerable increase in resting energy expenditure and substantial whole-body catabolism. In burned patients, the length and magnitude of the hypermetabolic state is the highest of all patients and associated with profoundly increased morbidity and mortality. Unfortunately, the mechanisms involved in hypermetabolism are essentially unknown. We hypothesized that the adipose tissue plays a central role for the induction and persistence of hypermetabolism post-burn injury. Here, we show that burn induces a switch in the phenotype of the subcutaneous fat from white to beige, with associated characteristics such as increased mitochondrial mass and UCP1 expression. Our results further demonstrate the significant role of catecholamines and interleukin-6 in this process. We conclude that subcutaneous fat remodeling and browning represent an underlying mechanism that explains the elevated energy expenditure in burn-induced hypermetabolism.

Indexed as

Adipose Tissue, WhiteAnimalsBurnsCatecholaminesEnergy MetabolismFemaleHumansInterleukin-6Ion ChannelsMaleMiceMice, Inbred C57BLMiddle AgedMitochondriaMitochondrial ProteinsUncoupling Protein 1CatecholaminesInterleukin-6Ion ChannelsMitochondrial ProteinsUCP1 protein, humanUcp1 protein, mouseUncoupling Protein 1

Identifiers

PMID26586436
PMCPMC4662886

What OpenQuestion holds

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Registered trials

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 OpenQuestion graph.