Evidence map›Paper›PMID 29746591›Full record

ArticlePloS one2018

Brown adipose tissue plays a central role in systemic inflammation-induced sleep responses.

Éva Szentirmai, Levente Kapás

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
  2. Review
  3. Metabolic signals in sleep regulation: the role of brown adipose tissue.Neurobiology of sleep and circadian rhythms · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. The Causal Relationship Between Sleep and Obesity: Novel Insights and Therapeutic Target.The Journal of clinical endocrinology and metabolism · 2022
    Article
  11. Article
  12. Article
  13. Sleep and thermoregulation.Current opinion in physiology · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. The Temperature Dependence of Sleep.Frontiers in neuroscience · 2019
    Review
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

2 authors at 1 institution in 1 country.

Éva SzentirmaiElson S. Floyd College of Medicine, Department of Biomedical Sciences, Washington State University, Spokane, Washington, United States of America.ORCID 0000-0001-7708-815X
Levente KapásElson S. Floyd College of Medicine, Department of Biomedical Sciences, Washington State University, Spokane, Washington, United States of America.
Washington State University Spokane · US

Funding

Brown Adipose Tissue and Sleep RegulationR01HL122390 · NHLBI · WASHINGTON STATE UNIVERSITY · PI SZENTIRMAI, EVA · 2015 to 2019
$1.9M
NHLBI NIH HHS R01 HL122390
6 · The paper itself

Abstract

We previously identified brown adipose tissue (BAT) as a source of sleep-inducing signals. Pharmacological activation of BAT enhances sleep while sleep loss leads to increased BAT thermogenesis. Recovery sleep after sleep loss is diminished in mice that lack uncoupling protein 1 (UCP-1), and also in wild-type (WT) mice after sensory denervation of the BAT. Systemic inflammation greatly affects metabolism and the function of adipose tissue, and also induces characteristic sleep responses. We hypothesized that sleep responses to acute inflammation are mediated by BAT-derived signals. To test this, we determined the effects of systemic inflammation on sleep and body temperature in UCP-1 knockout (KO) and WT mice. Intraperitoneal injections of lipopolysaccharide, tumor necrosis factor-α, interleukin-1 beta and clodronate containing liposomes were used to induce systemic inflammation. In WT animals, non-rapid-eye movement sleep (NREMS) was elevated in all four inflammatory models. All NREMS responses were completely abolished in UCP-1 KO animals. Systemic inflammation elicited an initial hypothermia followed by fever in WT mice. The hypothermic phase, but not the fever, was abolished in UCP-1 KO mice. The only recognized function of UCP-1 is to promote thermogenesis in brown adipocytes. Present results indicate that the presence of UCP-1 is necessary for increased NREMS but does not contribute to the development of fever in systemic inflammation.

Indexed as

InflammationAdipocytes, BrownAdipose Tissue, BrownAnimalsBody TemperatureClodronic AcidElectroencephalographyElectromyographyGenotypeInterleukin-1betaIon ChannelsLipopolysaccharidesLiposomesMaleMiceMice, Inbred C57BLClodronic AcidInterleukin-1betaIon ChannelsLipopolysaccharidesLiposomesMitochondrial ProteinsTumor Necrosis Factor-alphaUncoupling Protein 1

Identifiers

PMID29746591
PMCPMC5945014
OpenAlexW2801273198

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.