Evidence map›Paper›PMID 22615911›Full record

ArticlePloS one2012

PCB 126 and other dioxin-like PCBs specifically suppress hepatic PEPCK expression via the aryl hydrocarbon receptor.

Wenshuo Zhang, Robert M Sargis, Paul A Volden, Christopher M Carmean, Xiao J Sun, Matthew J Brady

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 115 citations in OpenAlex.

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  19. Microbial and enzymatic degradation of PCBs from e-waste-contaminated sites: a review.Environmental science and pollution research international · 2021
    Review
  20. Article

3 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Wenshuo ZhangDepartment of Medicine, Kovler Center for Biomedical Discovery, The University of Chicago, Chicago, Illinois, United States of America.
Robert M Sargis
Paul A Volden
Christopher M Carmean
Xiao J Sun
Matthew J Brady
University of Chicago · USUniversity of Maryland, Baltimore · US

Funding

Environmental Endocrine Disruption of Adipocyte MetabolismK08ES019176 · NIEHS · UNIVERSITY OF CHICAGO · PI SARGIS, ROBERT M · 2010 to 2014
$797k
Environmental Endocrine Disruptors and Adipocyte BiologyF32ES017397 · NIEHS · UNIVERSITY OF CHICAGO · PI SARGIS, ROBERT M · 2009 to 2009
$53k
NIEHS NIH HHS F32 ES017397NIEHS NIH HHS F32-ES017397NIEHS NIH HHS K08 ES019176NIEHS NIH HHS K08-ES019176
6 · The paper itself

Abstract

Dioxins and dioxin-like compounds encompass a group of structurally related heterocyclic compounds that bind to and activate the aryl hydrocarbon receptor (AhR). The prototypical dioxin is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a highly toxic industrial byproduct that incites numerous adverse physiological effects. Global commercial production of the structurally similar polychlorinated biphenyls (PCBs), however, commenced early in the 20(th) century and continued for decades; dioxin-like PCBs therefore contribute significantly to total dioxin-associated toxicity. In this study, PCB 126, the most potent dioxin-like PCB, was evaluated with respect to its direct effects on hepatic glucose metabolism using primary mouse hepatocytes. Overnight treatment with PCB 126 reduced hepatic glycogen stores in a dose-dependent manner. Additionally, PCB 126 suppressed forskolin-stimulated gluconeogenesis from lactate. These effects were independent of acute toxicity, as PCB 126 did not increase lactate dehydrogenase release nor affect lipid metabolism or total intracellular ATP. Interestingly, provision of cells with glycerol instead of lactate as the carbon source completely restored hepatic glucose production, indicating specific impairment in the distal arm of gluconeogenesis. In concordance with this finding, PCB 126 blunted the forskolin-stimulated increase in phosphoenolpyruvate carboxykinase (PEPCK) mRNA levels without affecting glucose-6-phosphatase expression. Myricetin, a putative competitive AhR antagonist, reversed the suppression of PEPCK induction by PCB 126. Furthermore, other dioxin-like PCBs demonstrated similar effects on PEPCK expression in parallel with their ability to activate AhR. It therefore appears that AhR activation mediates the suppression of PEPCK expression by dioxin-like PCBs, suggesting a role for these pollutants as disruptors of energy metabolism.

Indexed as

Adenosine TriphosphateAnimalsDioxinsFlavonoidsGene ExpressionGluconeogenesisGlucoseGlucose-6-PhosphataseGlycogenHepatocytesLactic AcidLiverL-Lactate DehydrogenaseMaleMiceMice, Inbred C57BL3,4,5,3',4'-pentachlorobiphenylAdenosine TriphosphateDioxinsFlavonoidsGlucoseGlucose-6-PhosphataseGlycogenLactic AcidL-Lactate DehydrogenasemyricetinPhosphoenolpyruvate CarboxylasePolychlorinated BiphenylsReceptors, Aryl Hydrocarbon

Identifiers

PMID22615911
PMCPMC3353882
OpenAlexW2027102959

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.