Soluble epoxide hydrolase is an endogenous regulator of obesity-induced intestinal barrier dysfunction and bacterial translocation
Open accessAbstract
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.
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Pharmacological inhibition of sEH prevented obesity-induced gut barrier dysfunction.
“Pharmacological inhibition of sEH (trans-4-(4-[3-(4-trifluoromethoxyphenyl) ureido] cyclohexyloxy) benzoic acid (t-TUCB), prevented obesity-induced gut barrier dysfunction suggesting sEH inhibitors may be promising agents for gut barrier dysfunction treatment in obesity conditions.199”
From Regulation of Intestinal Barrier Function by Microbial Metabolites (2021) · cites this paper as [199]
Increased expression of sEH led to enhanced gut permeability in diet-induced obesity models.
“It was demonstrated that increased expression of sEH led to enhanced gut permeability in diet-induced obesity models.199”
From Regulation of Intestinal Barrier Function by Microbial Metabolites (2021) · cites this paper as [199]
Genetic deletion of sEH (sEH knockout mice) abolished obesity-induced gut leakage, endotoxin lipopolysaccharide and bacterial translocation.
“Further, genetic deletion of sEH (sEH knockout mice) abolished obesity-induced gut leakage, endotoxin lipopolysaccharide and bacterial translocation.199”
From Regulation of Intestinal Barrier Function by Microbial Metabolites (2021) · cites this paper as [199]
Soluble epoxide hydrolase (sEH) and its metabolites (as dihydroxyeicosatrienoic acids) were upregulated in the colon tissues of diet-induced obese mice.
“Studies have shown that soluble epoxide hydrolase (sEH) and its metabolites (as dihydroxyeicosatrienoic acids) were upregulated in the colon tissues of diet-induced obese mice.”
From Regulation of Intestinal Barrier Function by Microbial Metabolites (2021) · cites this paper as [199]
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- Authors
- Wang, Y., Yang, J., Wang, W., Sanidad, K. Z., Cinelli, M. A., Wan, D., Hwang, S. H., Kim, D., Lee, K. S. S., Xiao, H., Hammock, B. D., & Zhang, G.
- Affiliations
- University of Massachusetts Amherst (US)
- UC Davis Comprehensive Cancer Center (US)
- Michigan State University (US)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2020-03-27
- Volume
- 117
- Issue
- 15
- Pages
- 8431-8436
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC7165420
- OpenAlex
- W3012957833
- Cited by
- 59
- References
- 24
- Citations by year
- 2026: 6 · 2025: 8 · 2024: 11 · 2023: 12 · 2022: 11 · 2021: 6 · 2020: 4 · 2019: 1
- FWCI
- 2.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- USDA | National Institute of Food and Agriculture (2016-67017-24423, 2019-67017-29248, MAS00492)
- HHS | NIH | National Cancer Institute (R03CA218520, R03CA237795)
- HHS | NIH | National Institute of Environmental Health Sciences (R35ES030443, P42ES004699, R00ES024806)
- NSF | MPS | Division of Mathematical Sciences (1761320)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- soluble epoxide hydrolase, obesity, intestinal barrier dysfunction, bacterial translocation, leaky gut, lipopolysaccharide, endotoxin, adipose tissue inflammation, dihydroxyeicosatrienoic acids, gut microbiota, colonic inflammation, sEH inhibitors, therapeutic target
- MeSH terms
- Gastrointestinal Microbiome, Adipose Tissue, Animals, Bacteria, Epoxide Hydrolases, Humans, Intestinal Diseases, Intestines, Male, Mice, Inbred C57BL, Obesity, Mice, Knockout, Bacterial Physiological Phenomena, Bacterial Translocation, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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