Evidence map›Paper›PMID 26865635›Full record

ArticleThe Journal of biological chemistry2016

Aryl Hydrocarbon Receptor Plays Protective Roles against High Fat Diet (HFD)-induced Hepatic Steatosis and the Subsequent Lipotoxicity via Direct Transcriptional Regulation of Socs3 Gene Expression.

Taira Wada, Hiroshi Sunaga, Kazuki Miyata, Haruno Shirasaki, Yuki Uchiyama, Shigeki Shimba

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.0field-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

49 citing papers in PubMed, 82 citations in OpenAlex.

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  15. Effects ofEnvironmental science & technology · 2023
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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

6 authors at 1 institution in 1 country.

Taira WadaFrom the Department of Health Science, School of Pharmacy, Nihon University, Funabashi, Chiba 274-8555, Japan.
Hiroshi SunagaFrom the Department of Health Science, School of Pharmacy, Nihon University, Funabashi, Chiba 274-8555, Japan.
Kazuki MiyataFrom the Department of Health Science, School of Pharmacy, Nihon University, Funabashi, Chiba 274-8555, Japan.
Haruno ShirasakiFrom the Department of Health Science, School of Pharmacy, Nihon University, Funabashi, Chiba 274-8555, Japan.
Yuki UchiyamaFrom the Department of Health Science, School of Pharmacy, Nihon University, Funabashi, Chiba 274-8555, Japan.
Shigeki ShimbaFrom the Department of Health Science, School of Pharmacy, Nihon University, Funabashi, Chiba 274-8555, Japan shimba.shigeki@nihon-u.ac.jp.
Nihon University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor regulating the expression of genes involved in xenobiotic response. Recent studies have suggested that AhR plays essential roles not only in xenobiotic detoxification but also energy metabolism. Thus, in this study, we studied the roles of AhR in lipid metabolism. Under high fat diet (HFD) challenge, liver-specific AhR knock-out (AhR LKO) mice exhibited severe steatosis, inflammation, and injury in the liver. Gene expression analysis and biochemical study revealed thatde novolipogenesis activity was significantly increased in AhR LKO mice. In contrast, induction of suppressor of cytokine signal 3 (Socs3) expression by HFD was attenuated in the livers of AhR LKO mice. Rescue of theSocs3gene in the liver of AhR LKO mice cancelled the HFD-induced hepatic lipotoxicities. Promoter analysis established Socs3 as novel transcriptional target of AhR. These results indicated that AhR plays a protective role against HFD-induced hepatic steatosis and the subsequent lipotoxicity effects, such as inflammation, and that the mechanism of protection involves the direct transcriptional regulation ofSocs3expression by AhR.

Indexed as

Diet, High-FatAnimalsBasic Helix-Loop-Helix ProteinsBinding SitesDietary FatsFatty LiverGene Expression RegulationLipid MetabolismLiverMaleMiceMice, Inbred C57BLMice, KnockoutPromoter Regions, GeneticProtein BindingReceptors, Aryl HydrocarbonAhr protein, mouseBasic Helix-Loop-Helix ProteinsDietary FatsReceptors, Aryl HydrocarbonSocs3 protein, mouseSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling Proteinsaryl hydrocarbon receptor (AhR)inflammationlipid metabolismliverliver injuryliver metabolismsuppressor of cytokine signal 3 (Socs3)

Identifiers

PMID26865635
PMCPMC4807284
OpenAlexW2254041544

What OpenQuestion holds

Textmetadata
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.