Evidence map›Paper›PMID 32831531›Full record

ArticleMedicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents2020

Dioxin-like and non-dioxin-like PCBs differentially regulate the hepatic proteome and modify diet-induced nonalcoholic fatty liver disease severity.

Jian Jin, Banrida Wahlang, Hongxue Shi, Josiah E Hardesty, K Cameron Falkner, Kimberly Z Head, Sudhir Srivastava, Michael L Merchant, Shesh N Rai, Matthew C Cave and 1 more

Abstract read
In one paragraph

Article in Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

30 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

11 authors.

Jian JinDepartment of Pharmacology & Toxicology, School of Medicine, University of Louisville, Louisville, KY, 40202, USA.
Banrida WahlangDivision of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, School of Medicine, University of Louisville, Louisville, KY, 40202, USA.
Hongxue ShiDepartment of Pharmacology & Toxicology, School of Medicine, University of Louisville, Louisville, KY, 40202, USA.
Josiah E HardestyDivision of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, School of Medicine, University of Louisville, Louisville, KY, 40202, USA.
K Cameron FalknerDivision of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, School of Medicine, University of Louisville, Louisville, KY, 40202, USA.
Kimberly Z HeadDivision of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, School of Medicine, University of Louisville, Louisville, KY, 40202, USA.
Sudhir SrivastavaDepartment of Bioinformatics and Biostatistics, School of Public Health and Information Sciences, University of Louisville, Louisville, KY, 40202, USA.
Michael L MerchantUofL Superfund Research Center, University of Louisville, Louisville, KY, 40202, USA.
Shesh N RaiUofL Superfund Research Center, University of Louisville, Louisville, KY, 40202, USA.
Matthew C CaveDepartment of Pharmacology & Toxicology, School of Medicine, University of Louisville, Louisville, KY, 40202, USA.
Russell A ProughDepartment of Biochemistry & Molecular Genetics, School of Medicine, University of Louisville, Louisville, KY, 40202, USA.

Funding

Role of oxidized linoleic acid metabolites in the pathogenesis of alcoholic liver diseaseP20GM113226 · NIGMS · UNIVERSITY OF LOUISVILLE · PI ZHANG, XIANG · 2016 to 2025
$24.1M
Superfund Training CoreP42ES023716 · NIEHS · UNIVERSITY OF LOUISVILLE · PI HEIN, DAVID W · 2017 to 2025
$18.1M
The Role of Nutrition in the Development/Progression of Alcohol-Induced Organ InjuryP50AA024337 · NIAAA · UNIVERSITY OF LOUISVILLE · PI CRAIG J. MCCLAIN · 2016 to 2026
$17.9M
UOFL ENVIRONMENTAL HEALTH SCIENCES TRAINING PROGRAMT32ES011564 · NIEHS · UNIVERSITY OF LOUISVILLE · PI David W Hein, John Pierce Wise · 2004 to 2026
$7.1M
Environmental Liver DiseaseR35ES028373 · NIEHS · UNIVERSITY OF LOUISVILLE · PI CAVE, MATTHEW C · 2017 to 2024
$4.0M
Exposome and Precision Medicine in NAFLDR01ES032189 · NIEHS · UNIVERSITY OF LOUISVILLE · PI CAVE, MATTHEW C · 2020 to 2022
$1.9M
RvD1-FPR2 signaling ameliorates alcoholic liver diseaseF32AA027950 · NIAAA · UNIVERSITY OF LOUISVILLE · PI HARDESTY, JOSIAH E · 2020 to 2022
$164k
NIAAA NIH HHS F32 AA027950NIAAA NIH HHS L30 AA027913NIAAA NIH HHS P50 AA024337NIEHS NIH HHS P42 ES023716NIEHS NIH HHS R01 ES032189NIEHS NIH HHS R35 ES028373NIEHS NIH HHS T32 ES011564NIGMS NIH HHS P20 GM113226
6 · The paper itself

Abstract

Polychlorinated biphenyls (PCBs) are persistent organic pollutants associated with metabolic disruption and non-alcoholic fatty liver disease (NAFLD). Based on their ability to activate the aryl hydrocarbon receptor (AhR), PCBs are subdivided into two classes: dioxin-like (DL) and non-dioxin-like (NDL) PCBs. Previously, we demonstrated that NDL PCBs compromised the liver to promote more severe diet-induced NAFLD. Here, the hepatic effects and potential mechanisms (by untargeted liver proteomics) of DL PCBs, NDL PCBs or co-exposure to both in diet-induced NAFLD are investigated. Male C57Bl/6 mice were fed a 42% fat diet and exposed to vehicle control; Aroclor1260 (20 mg/kg, NDL PCB mixture); PCB126 (20 μg/kg, DL PCB congener); or a mixture of Aroclor1260 (20 mg/kg)+PCB126 (20 μg/kg) for 12 weeks. Each exposure was associated with a distinct hepatic proteome. Phenotypic and proteomic analyses revealed increased hepatic inflammation and phosphoprotein signaling disruption by Aroclor1260. PCB126 decreased hepatic inflammation and fibrosis at the molecular level; while altering cytoskeletal remodeling, metal homeostasis, and intermediary/xenobiotic metabolism. PCB126 attenuated Aroclor1260-induced hepatic inflammation but increased hepatic free fatty acids in the co-exposure group. Aroclor1260+PCB126 exposure was strongly associated with multiple epigenetic processes, and these could potentially explain the observed non-additive effects of the exposures on the hepatic proteome. Taken together, the results demonstrated that PCB exposures differentially regulated the hepatic proteome and the histologic severity of diet-induced NAFLD. Future research is warranted to determine the AhR-dependence of the observed effects including metal homeostasis and the epigenetic regulation of gene expression.

Indexed as

Aroclor1260NAFLDPCB126PCBsproteomicsTASH

Identifiers

PMID32831531
PMCPMC7440142

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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.