Evidence map›Paper›PMID 30789748›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2019

Inhibition of soluble epoxide hydrolase ameliorates hyperhomocysteinemia-induced hepatic steatosis by enhancing β-oxidation of fatty acid in mice.

Liu Yao, Boyang Cao, Qian Cheng, Wenbin Cai, Chenji Ye, Jing Liang, Wenli Liu, Lu Tan, Meng Yan, Bochuan Li and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

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  15. Soluble epoxide hydrolase inhibitor, TPPU, increases regulatory T cells pathway in an arthritis model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
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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 4 institutions in 2 countries.

Liu YaoTianjin Key Laboratory of Metabolic Diseases; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education); Collaborative Innovation Center of Tianjin for Medical Epigenetics and Department of Physiology and Pathophysiology, Tianjin Medical University , Tianjin , China.
Boyang CaoTianjin Key Laboratory of Metabolic Diseases; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education); Collaborative Innovation Center of Tianjin for Medical Epigenetics and Department of Physiology and Pathophysiology, Tianjin Medical University , Tianjin , China.
Qian ChengTianjin Key Laboratory of Metabolic Diseases; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education); Collaborative Innovation Center of Tianjin for Medical Epigenetics and Department of Physiology and Pathophysiology, Tianjin Medical University , Tianjin , China.
Wenbin CaiTianjin Key Laboratory of Metabolic Diseases; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education); Collaborative Innovation Center of Tianjin for Medical Epigenetics and Department of Physiology and Pathophysiology, Tianjin Medical University , Tianjin , China.
Chenji YeTianjin Key Laboratory of Metabolic Diseases; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education); Collaborative Innovation Center of Tianjin for Medical Epigenetics and Department of Physiology and Pathophysiology, Tianjin Medical University , Tianjin , China.
Jing LiangTianjin Key Laboratory of Metabolic Diseases; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education); Collaborative Innovation Center of Tianjin for Medical Epigenetics and Department of Physiology and Pathophysiology, Tianjin Medical University , Tianjin , China.
Wenli LiuTianjin Key Laboratory of Metabolic Diseases; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education); Collaborative Innovation Center of Tianjin for Medical Epigenetics and Department of Physiology and Pathophysiology, Tianjin Medical University , Tianjin , China.
Lu TanDepartment of Laboratory Animal Science and Technology, Tianjin Medical University , Tianjin , China.
Meng YanTianjin Key Laboratory of Metabolic Diseases; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education); Collaborative Innovation Center of Tianjin for Medical Epigenetics and Department of Physiology and Pathophysiology, Tianjin Medical University , Tianjin , China.
Bochuan LiTianjin Key Laboratory of Metabolic Diseases; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education); Collaborative Innovation Center of Tianjin for Medical Epigenetics and Department of Physiology and Pathophysiology, Tianjin Medical University , Tianjin , China.
Jinlong HeTianjin Key Laboratory of Metabolic Diseases; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education); Collaborative Innovation Center of Tianjin for Medical Epigenetics and Department of Physiology and Pathophysiology, Tianjin Medical University , Tianjin , China.
Sung Hee HwangDepartment of Entomology and Nematology and University of California, Davis Comprehensive Cancer Center , Davis, California.
Xu ZhangTianjin Key Laboratory of Metabolic Diseases; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education); Collaborative Innovation Center of Tianjin for Medical Epigenetics and Department of Physiology and Pathophysiology, Tianjin Medical University , Tianjin , China.
Chunjiong WangTianjin Key Laboratory of Metabolic Diseases; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education); Collaborative Innovation Center of Tianjin for Medical Epigenetics and Department of Physiology and Pathophysiology, Tianjin Medical University , Tianjin , China.
Ding AiTianjin Key Laboratory of Metabolic Diseases; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education); Collaborative Innovation Center of Tianjin for Medical Epigenetics and Department of Physiology and Pathophysiology, Tianjin Medical University , Tianjin , China.
Bruce D HammockDepartment of Entomology and Nematology and University of California, Davis Comprehensive Cancer Center , Davis, California.
Yi ZhuTianjin Key Laboratory of Metabolic Diseases; Key Laboratory of Immune Microenvironment and Disease (Ministry of Education); Collaborative Innovation Center of Tianjin for Medical Epigenetics and Department of Physiology and Pathophysiology, Tianjin Medical University , Tianjin , China.
Tianjin Medical University · CNTianjin Infectious Diseases Hospital · CNUC Davis Comprehensive Cancer CenterUniversity of California, Davis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic steatosis is the beginning phase of nonalcoholic fatty liver disease, and hyperhomocysteinemia (HHcy) is a significant risk factor. Soluble epoxide hydrolase (sEH) hydrolyzes epoxyeicosatrienoic acids (EETs) and other epoxy fatty acids, attenuating their cardiovascular protective effects. However, the involvement of sEH in HHcy-induced hepatic steatosis is unknown. The current study aimed to explore the role of sEH in HHcy-induced lipid disorder. We fed 6-wk-old male mice a chow diet or 2% (wt/wt) high-metnionine diet for 8 wk to establish the HHcy model. A high level of homocysteine induced lipid accumulation in vivo and in vitro, which was concomitant with the increased activity and expression of sEH. Treatment with a highly selective specific sEH inhibitor (0.8 mg·kg

Indexed as

Epoxide HydrolasesFatty LiverHyperhomocysteinemiaAnimalsDisease Models, AnimalDrug DiscoveryEnzyme InhibitorsFatty AcidsLigandsMiceMice, Inbred C57BLPPAR alphaUp-RegulationEnzyme InhibitorsEpoxide HydrolasesFatty AcidsLigandsPPAR alphahepatocyteshyperhomocysteinemiaproliferator-activated receptor-αsoluble epoxide hydrolaseβ-oxidation

Identifiers

PMID30789748
PMCPMC6483021
OpenAlexW2916244874

What Socratic 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 Socratic graph.