Evidence map›Paper›PMID 32220957›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

Soluble epoxide hydrolase is an endogenous regulator of obesity-induced intestinal barrier dysfunction and bacterial translocation.

Yuxin Wang, Jun Yang, Weicang Wang, Katherine Z Sanidad, Maris A Cinelli, Debin Wan, Sung Hee Hwang, Daeyoung Kim, Kin Sing Stephen Lee, Hang Xiao and 2 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  5. Review
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  7. Intravital imaging of translocated bacteria via fluorogenic labeling of gut microbiota in situ.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. Effect ofFrontiers in microbiology · 2025
    Article
  11. Metabolomics reveals soluble epoxide hydrolase as a therapeutic target for high-sucrose diet-mediated gut barrier dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. Article
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  14. c-Jun N-terminal kinase signaling in aging.Frontiers in aging neuroscience · 2024
    Review
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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

12 authors at 3 institutions in 2 countries.

Yuxin WangCollege of Life Sciences, Northwest University, Xi'an 710069, China.
Jun YangDepartment of Entomology and Nematology and UC Davis Comprehensive Cancer Center, University of California, Davis, CA 95817.
Weicang WangDepartment of Food Science, University of Massachusetts, Amherst, MA 01003.
Katherine Z SanidadDepartment of Food Science, University of Massachusetts, Amherst, MA 01003.
Maris A CinelliDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824.
Debin WanDepartment of Entomology and Nematology and UC Davis Comprehensive Cancer Center, University of California, Davis, CA 95817.
Sung Hee HwangDepartment of Entomology and Nematology and UC Davis Comprehensive Cancer Center, University of California, Davis, CA 95817.
Daeyoung KimDepartment of Mathematics and Statistics, University of Massachusetts, Amherst, MA 01003.
Kin Sing Stephen LeeDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824.
Hang XiaoDepartment of Food Science, University of Massachusetts, Amherst, MA 01003.
Bruce D HammockDepartment of Entomology and Nematology and UC Davis Comprehensive Cancer Center, University of California, Davis, CA 95817; bdhammock@ucdavis.edu guodongzhang@umass.edu.ORCID 0000-0003-1408-8317
Guodong ZhangDepartment of Food Science, University of Massachusetts, Amherst, MA 01003; bdhammock@ucdavis.edu guodongzhang@umass.edu.ORCID 0000-0001-7780-5470
University of Massachusetts Amherst · USUC Davis Comprehensive Cancer CenterMichigan State University · US

Funding

Workshop on Environmental Technology Transfer and EntrepreneurshipP42ES004699 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1987 to 2021
$50.1M
Supplement for bioactive lipids as effectors and indicators of the deleterious effects of human healthR35ES030443 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI MORISSEAU, CHRISTOPHE HP · 2019 to 2025
$5.8M
Identifying the receptors of environmentally sensitive epoxy-eicosanoids with AMSR00ES024806 · NIEHS · MICHIGAN STATE UNIVERSITY · PI LEE, KIN SING STEPHEN · 2017 to 2019
$727k
Prevention of obesity-enhanced colorectal cancer via targeting soluble epoxide hydrolaseR03CA237795 · NCI · UNIVERSITY OF MASSACHUSETTS AMHERST · PI DECKER, ERIC · 2019 to 2020
$147k
Prevention of colorectal cancer via targeting CYP epoxygenasesR03CA218520 · NCI · UNIVERSITY OF MASSACHUSETTS AMHERST · PI ZHANG, GUODONG · 2018 to 2019
$147k
NCI NIH HHS R03 CA218520NCI NIH HHS R03 CA237795NIEHS NIH HHS P42 ES004699NIEHS NIH HHS R00 ES024806NIEHS NIH HHS R35 ES030443
6 · The paper itself

Abstract

Intestinal barrier dysfunction, which leads to translocation of bacteria or toxic bacterial products from the gut into bloodstream and results in systemic inflammation, is a key pathogenic factor in many human diseases. However, the molecular mechanisms leading to intestinal barrier defects are not well understood, and there are currently no available therapeutic approaches to target intestinal barrier function. Here we show that soluble epoxide hydrolase (sEH) is an endogenous regulator of obesity-induced intestinal barrier dysfunction. We find that sEH is overexpressed in the colons of obese mice. In addition, pharmacologic inhibition or genetic ablation of sEH abolishes obesity-induced gut leakage, translocation of endotoxin lipopolysaccharide or bacteria, and bacterial invasion-induced adipose inflammation. Furthermore, systematic treatment with sEH-produced lipid metabolites, dihydroxyeicosatrienoic acids, induces bacterial translocation and colonic inflammation in mice. The actions of sEH are mediated by gut bacteria-dependent mechanisms, since inhibition or genetic ablation of sEH fails to attenuate obesity-induced gut leakage and adipose inflammation in mice lacking gut bacteria. Overall, these results support that sEH is a potential therapeutic target for obesity-induced intestinal barrier dysfunction, and that sEH inhibitors, which have been evaluated in human clinical trials targeting other human disorders, could be promising agents for prevention and/or treatment.

Indexed as

Bacterial TranslocationAdipose TissueAnimalsBacteriaBacterial Physiological PhenomenaEpoxide HydrolasesGastrointestinal MicrobiomeHumansIntestinal DiseasesIntestinesMaleMiceMice, Inbred C57BLMice, KnockoutObesityEphx2 protein, mouseEpoxide Hydrolasesintestinal barrier dysfunctionobesitysoluble epoxide hydrolase

Identifiers

PMID32220957
PMCPMC7165420
OpenAlexW3012957833

What OpenQuestion holds

Textmetadata
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.