Evidence map›Paper›PMID 32577122›Full record

ArticleNutrition & metabolism2020

TET1 promotes fatty acid oxidation and inhibits NAFLD progression by hydroxymethylation of PPARα promoter.

Jingjie Wang, Yitong Zhang, Qin Zhuo, Yujen Tseng, Jiucun Wang, Yanyun Ma, Jun Zhang, Jie Liu

Open access · goldAbstract read
In one paragraph

Article in Nutrition & metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.2field-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

25 citing papers in PubMed, 36 citations in OpenAlex.

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  16. Mechanism and therapeutic strategy of hepaticWorld journal of gastroenterology · 2022
    Article
  17. Antidiabetic Effect ofBioMed research international · 2022
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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

8 authors at 2 institutions in 1 country.

Jingjie Wang *Department of Digestive Diseases of Huashan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Yitong Zhang *Department of Digestive Diseases of Huashan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Qin Zhuo *Department of Digestive Diseases of Huashan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Yujen TsengDepartment of Digestive Diseases of Huashan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Jiucun WangState Key Laboratory of Genetic Engineering, Human Phenome Institute, Fudan University, Shanghai, China.
Yanyun MaState Key Laboratory of Genetic Engineering, Human Phenome Institute, Fudan University, Shanghai, China.
Jun ZhangDepartment of Digestive Diseases of Huashan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Jie LiuDepartment of Digestive Diseases of Huashan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Fudan University · CNHuashan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAs a lipid metabolic disorder, non-alcoholic fatty liver disease (NAFLD) is an important cause of cirrhosis and hepatocellular carcinoma, with no effective drug up to date. Previous studies have demonstrated increased methylation levels of key genes in NAFLD, suggesting that hydroxymethylation, a key step in demethylation, may be a possible strategy to reverse NAFLD. TET1 is well known as a key hydroxymethylase, however, its role and mechanism in NAFLD remains unclear.

methodsIn this study, we utilized TET1 knockout mice, fed with high-fat diet. Furthermore, by ChIP and hMeDIP. TET1 knockdown L02 and HepG2 cell lines.

resultsTheir degree of liver steatosis was more severe than that of wild-type mice, suggesting that TET1 had a significant protective effect against NAFLD. We further found that PPARα, a key regulator of fatty acid oxidation, and its downstream key enzymes ACOX1 and CPT1A, as well as the fatty acid oxidation product β-HB were significantly decreased in TET1 knockout mice. While the key genes for fatty acid synthesis and uptake were not significantly changed, suggesting that TET1 inhibits NAFLD by promoting fatty acid oxidation via PPARα pathway. TET1 was confirmed to directly bind to the promoter of PPARα and elevate its hydroxymethylation level.

conclusionsThis study is the first to show that TET1 can activate PPARα, promote fatty acid oxidation and inhibit NAFLD progression by hydroxymethylation of PPARα promoter, which may be a new strategy to reverse NAFLD.

Indexed as

Fatty acid oxidationHydroxymethylationNAFLDPPARαTET1

Identifiers

PMID32577122
PMCPMC7304222
OpenAlexW3036259559

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.