Evidence map›Paper›PMID 37487068›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2023

NFIA in adipocytes reciprocally regulates mitochondrial and inflammatory gene program to improve glucose homeostasis.

Yuta Hiraike, Kaede Saito, Misato Oguchi, Takahito Wada, Gotaro Toda, Shuichi Tsutsumi, Kana Bando, Junji Sagawa, Gaku Nagano, Haruya Ohno and 7 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

24 citing papers in PubMed, 25 citations in OpenAlex.

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  20. Enhanced ECCD36 signaling promotes skeletal muscle insulin resistance in female mice.American journal of physiology. Endocrinology and metabolism · 2024
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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

17 authors at 7 institutions in 1 country.

Yuta HiraikeDivision for Health Service Promotion, The University of Tokyo, Tokyo 113-0033, Japan.ORCID 0000-0001-9799-7975
Kaede SaitoDivision for Health Service Promotion, The University of Tokyo, Tokyo 113-0033, Japan.
Misato OguchiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Takahito WadaDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Gotaro TodaDepartment 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.
Kana BandoLaboratory for Animal Resources and Genetic Engineering, RIKEN Center for Biosystems Dynamics Research, Kobe 650-0047, Japan.
Junji SagawaDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8551, Japan.
Gaku NaganoDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8551, Japan.ORCID 0000-0003-0291-4669
Haruya OhnoDepartment of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8551, Japan.
Naoto KubotaDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Tetsuya KubotaDepartment 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.
Takashi KadowakiToranomon Hospital, Tokyo 105-8470, Japan.
Hironori WakiDepartment of Diabetes and Endocrinology, Akita University Graduate School of Medicine, Akita 010-8543, Japan.
Shintaro YanagimotoDivision for Health Service Promotion, The University of Tokyo, Tokyo 113-0033, 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 · JPNational Institute of Biomedical Innovation, Health and Nutrition · JPRIKEN Center for Biosystems Dynamics Research · JPToranomon Hospital · JPUniversity of Tokyo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adipose tissue is central to regulation of energy homeostasis. Adaptive thermogenesis, which relies on mitochondrial oxidative phosphorylation (Ox-Phos), dissipates energy to counteract obesity. On the other hand, chronic inflammation in adipose tissue is linked to type 2 diabetes and obesity. Here, we show that nuclear factor I-A (NFIA), a transcriptional regulator of brown and beige adipocytes, improves glucose homeostasis by upregulation of Ox-Phos and reciprocal downregulation of inflammation. Mice with transgenic expression of NFIA in adipocytes exhibited improved glucose tolerance and limited weight gain. NFIA up-regulates Ox-Phos and brown-fat-specific genes by enhancer activation that involves facilitated genomic binding of PPARγ. In contrast, NFIA in adipocytes, but not in macrophages, down-regulates proinflammatory cytokine genes to ameliorate adipose tissue inflammation. NFIA binds to regulatory region of the

Indexed as

Diabetes Mellitus, Type 2NFI Transcription FactorsAdipocytesAdipose Tissue, BrownAnimalsCytokinesHomeostasisHumansInflammationMiceCytokinesNFIA protein, humanNFI Transcription Factorsadipocytesdiabetesinflammationtranscription factor

Identifiers

PMID37487068
PMCPMC10401007
OpenAlexW4385191340

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.