Evidence map›Paper›PMID 35874098›Full record

ArticleiScience2022

NFIA determines the

Yuta Hiraike, Shuichi Tsutsumi, Takahito Wada, Misato Oguchi, Kaede Saito, Masahiro Nakamura, Satoshi Ota, Michinori Koebis, Harumi Nakao, Atsu Aiba and 8 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

3 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. NFIA in adipocytes reciprocally regulates mitochondrial and inflammatory gene program to improve glucose homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    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

18 authors at 4 institutions in 1 country.

Yuta HiraikeDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, the University of Tokyo, Tokyo 113-8655, Japan.
Shuichi TsutsumiGenome Science and Medicine Laboratory, Research Center for Advanced Science and Technology, the University of Tokyo, Tokyo 153-8904, Japan.
Takahito WadaDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, the University of Tokyo, Tokyo 113-8655, Japan.
Misato OguchiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, the University of Tokyo, Tokyo 113-8655, Japan.
Kaede SaitoDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, the University of Tokyo, Tokyo 113-8655, Japan.
Masahiro NakamuraPrecision Health, Department of Bioengineering, Graduate School of Engineering, the University of Tokyo, Tokyo 113-8655, Japan.
Satoshi OtaGenome Science and Medicine Laboratory, Research Center for Advanced Science and Technology, the University of Tokyo, Tokyo 153-8904, Japan.
Michinori KoebisLaboratory of Animal Resources, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, the University of Tokyo, Tokyo 113-0033, Japan.
Harumi NakaoLaboratory of Animal Resources, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, the University of Tokyo, Tokyo 113-0033, Japan.
Atsu AibaLaboratory of Animal Resources, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, the University of Tokyo, Tokyo 113-0033, Japan.
Gaku NaganoDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8551, Japan.
Haruya OhnoDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8551, Japan.
Kenji OkiDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8551, Japan.
Masayasu YonedaDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8551, Japan.
Takashi KadowakiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, the University of Tokyo, Tokyo 113-8655, Japan.
Hiroyuki AburataniGenome Science and Medicine Laboratory, Research Center for Advanced Science and Technology, the University of Tokyo, Tokyo 153-8904, Japan.
Hironori WakiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, the University of Tokyo, Tokyo 113-8655, Japan.
Toshimasa YamauchiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, the University of Tokyo, Tokyo 113-8655, Japan.
The University of Tokyo · JPHiroshima University · JPAkita University · JPToranomon Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thermogenic brown and beige adipocytes counteract obesity by enhancing energy dissipation via uncoupling protein-1 (Ucp1). However, the effect of genetic variation on these cells, a major source of disease susceptibility, has been less well studied. Here we examined beige adipocytes from obesity-prone C57BL/6J (B6) and obesity-resistant 129X1/SvJ (129) mouse strains and identified a

Indexed as

EpigeneticsMolecular biologyMolecular physiologyPhysiology

Identifiers

PMID35874098
PMCPMC9304612
OpenAlexW4284878937

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.