Evidence map›Paper›PMID 26023891›Full record

ArticleEnvironmental science & technology2015

Metabolomics Reveals that Aryl Hydrocarbon Receptor Activation by Environmental Chemicals Induces Systemic Metabolic Dysfunction in Mice.

Limin Zhang, Emmanuel Hatzakis, Robert G Nichols, Ruixin Hao, Jared Correll, Philip B Smith, Christopher R Chiaro, Gary H Perdew, Andrew D Patterson

Abstract read
In one paragraph

Article in Environmental science & technology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 91 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

9 authors at 2 institutions in 2 countries.

Limin Zhang†Center for Molecular Toxicology and Carcinogenesis, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16802, United States.
Emmanuel Hatzakis§Department of Chemistry, The Pennsylvania State University, University Park, Pennsylvania 16802, United States.
Robert G Nichols†Center for Molecular Toxicology and Carcinogenesis, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16802, United States.
Ruixin Hao†Center for Molecular Toxicology and Carcinogenesis, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16802, United States.
Jared Correll†Center for Molecular Toxicology and Carcinogenesis, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16802, United States.
Philip B Smith⊥Metabolomics Facility, The Huck Institutes of the Life Sciences, The Pennsylvania State University, University Park, Pennsylvania 16802, United States.
Christopher R Chiaro†Center for Molecular Toxicology and Carcinogenesis, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16802, United States.
Gary H Perdew†Center for Molecular Toxicology and Carcinogenesis, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16802, United States.
Andrew D Patterson†Center for Molecular Toxicology and Carcinogenesis, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16802, United States.
Pennsylvania State University · USChinese Academy of Sciences · CN

Funding

REGULATION OF THE AH RECEPTORR01ES004869 · NIEHS · PURDUE UNIVERSITY WEST LAFAYETTE · PI PERDEW, GARY H. · 1994 to 2017
$5.3M
Optimized Metabolite Extraction, Separation, and Identification for MetabolomicsR01ES022186 · NIEHS · PENNSYLVANIA STATE UNIVERSITY, THE · PI PATTERSON, ANDREW · 2012 to 2016
$2.0M
Selective Ah Receptor Ligands Repress Acute-Phase ResponseR01ES019964 · NIEHS · PENNSYLVANIA STATE UNIVERSITY, THE · PI PERDEW, GARY H. · 2012 to 2016
$2.0M
BIOCHEMICAL CHARACTERIZATION OF THE AH RECEPTORR29ES004869 · NIEHS · PURDUE UNIVERSITY WEST LAFAYETTE · PI PERDEW, GARY H · 1989 to 1993
–
NIEHS NIH HHS ES004869NIEHS NIH HHS ES019964NIEHS NIH HHS ES022186NIEHS NIH HHS R01 ES004869NIEHS NIH HHS R01 ES019964NIEHS NIH HHS R01 ES022186
6 · The paper itself

Abstract

Environmental exposure to dioxins and dioxin-like compounds poses a significant health risk for human health. Developing a better understanding of the mechanisms of toxicity through activation of the aryl hydrocarbon receptor (AHR) is likely to improve the reliability of risk assessment. In this study, the AHR-dependent metabolic response of mice exposed to 2,3,7,8-tetrachlorodibenzofuran (TCDF) was assessed using global (1)H nuclear magnetic resonance (NMR)-based metabolomics and targeted metabolite profiling of extracts obtained from serum and liver. (1)H NMR analyses revealed that TCDF exposure suppressed gluconeogenesis and glycogenolysis, stimulated lipogenesis, and triggered inflammatory gene expression in an Ahr-dependent manner. Targeted analyses using gas chromatography coupled with mass spectrometry showed TCDF treatment altered the ratio of unsaturated/saturated fatty acids. Consistent with this observation, an increase in hepatic expression of stearoyl coenzyme A desaturase 1 was observed. In addition, TCDF exposure resulted in inhibition of de novo fatty acid biosynthesis manifested by down-regulation of acetyl-CoA, malonyl-CoA, and palmitoyl-CoA metabolites and related mRNA levels. In contrast, no significant changes in the levels of glucose and lipid were observed in serum and liver obtained from Ahr-null mice following TCDF treatment, thus strongly supporting the important role of the AHR in mediating the metabolic effects seen following TCDF exposure.

Indexed as

AnimalsBenzofuransDioxinsEnvironmental PollutantsFatty AcidsGene ExpressionGlucoseLipid MetabolismLiverMagnetic Resonance SpectroscopyMaleMetabolomicsMiceMice, Inbred C57BLMice, Mutant StrainsReceptors, Aryl Hydrocarbon2,3,7,8-tetrachlorodibenzofuranBenzofuransDioxinsEnvironmental PollutantsFatty AcidsGlucoseReceptors, Aryl Hydrocarbon

Identifiers

PMID26023891
PMCPMC4890155
OpenAlexW2232265473

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.