Evidence map›Paper›PMID 30453990›Full record

ArticleJournal of translational medicine2018

Deficiency in interleukin-18 promotes differentiation of brown adipose tissue resulting in fat accumulation despite dyslipidemia.

Kyosuke Yamanishi, Seishi Maeda, Sachi Kuwahara-Otani, Takuya Hashimoto, Kaoru Ikubo, Keiichiro Mukai, Keiji Nakasho, Naomi Gamachi, Yosif El-Darawish, Wen Li and 5 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Molecular Mechanisms of IL18 in Disease.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Article
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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

15 authors at 3 institutions in 1 country.

Kyosuke YamanishiDepartment of Neuropsychiatry, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, 663-8501, Japan.
Seishi MaedaDepartment of Anatomy and Cell Biology, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, 663-8501, Japan.
Sachi Kuwahara-OtaniDepartment of Anatomy and Cell Biology, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, 663-8501, Japan.
Takuya HashimotoDepartment of Neuropsychiatry, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, 663-8501, Japan.
Kaoru IkuboDepartment of Neuropsychiatry, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, 663-8501, Japan.
Keiichiro MukaiDepartment of Neuropsychiatry, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, 663-8501, Japan.
Keiji NakashoDepartment of Pathology, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, 663-8501, Japan.
Naomi GamachiLaboratory of Tumor Immunology and Cell Therapy, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, 663-8501, Japan.
Yosif El-DarawishLaboratory of Tumor Immunology and Cell Therapy, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, 663-8501, Japan.
Wen LiLaboratory of Tumor Immunology and Cell Therapy, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, 663-8501, Japan.
Daisuke OkuzakiGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, 565-0871, Japan.
Yuko WatanabeHirakata General Hospital for Developmental Disorders, 2-1-1 Tsudahigashi, Hirakata, Osaka, 573-0122, Japan.
Hiromichi YamanishiHirakata General Hospital for Developmental Disorders, 2-1-1 Tsudahigashi, Hirakata, Osaka, 573-0122, Japan.
Haruki OkamuraLaboratory of Tumor Immunology and Cell Therapy, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, 663-8501, Japan.
Hisato MatsunagaDepartment of Neuropsychiatry, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo, 663-8501, Japan. hisa1311@hyo-med.ac.jp.ORCID 0000-0002-3724-3722
Hyogo Medical University · JPHiraka General Hospital · JPThe University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe cytokine, interleukin-18 (IL-18), was originally identified as an interferon-γ-inducing proinflammatory factor; however, there is increasing evidence suggesting that it has non-immunological effects on physiological functions. We have previously investigated the potential pathophysiological relationship between IL-18 and dyslipidemia, non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, which were mediated by lipid energy imbalance. Therefore, herein we focused on brown adipocytes (BAs) and brown adipose tissue (BAT) related to energy consumption as non-shivering thermogenesis.

methodsIl18

resultsCompared with Il18

conclusionsThis study demonstrated the critical function of IL-18 in differentiation and lipid metabolism in BAs. Furthermore, IL-18 may contribute to novel treatments by improving the energy imbalance.

Indexed as

AdiposityCell DifferentiationAdipogenesisAdipose Tissue, BrownAnimalsDyslipidemiasFatty LiverInterleukin-18Lipid MetabolismMaleMice, Inbred C57BLRecombinant ProteinsStem CellsThermogenesisInterleukin-18Recombinant ProteinsAdipogenesisBrown adipocytesBrown adipose tissueInterleukin-18Interleukin-18 knockoutLipid metabolism

Identifiers

PMID30453990
PMCPMC6245626
OpenAlexW2901070596

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.