Evidence map›Paper›PMID 26712468›Full record

ArticleToxicology and applied pharmacology2016

Bisphenol A sulfonation is impaired in metabolic and liver disease.

Emine B Yalcin, Supriya R Kulkarni, Angela L Slitt, Roberta King

Open access · greenAbstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 11% 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

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

  1. Pooled it
  2. Review
  3. Review
  4. Xenobiotic-Induced Aggravation of Metabolic-Associated Fatty Liver Disease.International journal of molecular sciences · 2022
    Review
  5. Observational
  6. The Role of Sulfotransferases in Liver Diseases.Drug metabolism and disposition: the biological fate of chemicals · 2020
    Review
  7. Article
  8. 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

4 authors at 1 institution in 1 country.

Emine B YalcinDepartment of Biomedical and Pharmaceutical Sciences, College of Pharmacy, University of Rhode Island, Kingston, RI, United States.
Supriya R KulkarniDepartment of Biomedical and Pharmaceutical Sciences, College of Pharmacy, University of Rhode Island, Kingston, RI, United States.
Angela L SlittDepartment of Biomedical and Pharmaceutical Sciences, College of Pharmacy, University of Rhode Island, Kingston, RI, United States. Electronic address: angela_slitt@uri.edu.
Roberta KingDepartment of Biomedical and Pharmaceutical Sciences, College of Pharmacy, University of Rhode Island, Kingston, RI, United States. Electronic address: rking@uri.edu.
University of Rhode Island · US

Funding

Training CoreP20GM103430 · NIGMS · UNIVERSITY OF RHODE ISLAND · PI Ang Cai · 2012 to 2026
$63.6M
Effect of nutritional status on MRP2 expression and biliary excretion of bisphenoR01ES016042 · NIEHS · UNIVERSITY OF RHODE ISLAND · PI SLITT, ANGELA L · 2008 to 2012
$2.4M
Developmental exposure to Bisphenol A and susceptibility to liver injuryR15ES025404 · NIEHS · UNIVERSITY OF RHODE ISLAND · PI SLITT, ANGELA L · 2015 to 2015
$439k
Role of Nrf2 during cholestsis and gallstone formationK22ES013782 · NIEHS · UNIVERSITY OF RHODE ISLAND · PI SLITT, ANGELA L · 2007 to 2009
$323k
NIDDK NIH HHS N01-DK-7-0004NIEHS NIH HHS K22 ES013782NIEHS NIH HHS K22ES013782NIEHS NIH HHS R01 ES016042NIEHS NIH HHS R01ES016042NIEHS NIH HHS R15 ES025404NIGMS NIH HHS 2 P20 GM103430NIGMS NIH HHS P20 GM103430NLM NIH HHS HHSN267200700004CNLM NIH HHS HHSN267200700004G
6 · The paper itself

Abstract

backgroundBisphenol A (BPA) is a widely used industrial chemical and suspected endocrine disruptor to which humans are ubiquitously exposed. The liver metabolizes and facilitates BPA excretion through glucuronidation and sulfonation. The sulfotransferase enzymes contributing to BPA sulfonation (detected in human and rodents) is poorly understood.

objectivesTo determine the impact of metabolic and liver disease on BPA sulfonation in human and mouse livers.

methodsThe capacity for BPA sulfonation was determined in human liver samples that were categorized into different stages of metabolic and liver disease (including obesity, diabetes, steatosis, and cirrhosis) and in livers from ob/ob mice.

resultsIn human liver tissues, BPA sulfonation was substantially lower in livers from subjects with steatosis (23%), diabetes cirrhosis (16%), and cirrhosis (18%), relative to healthy individuals with non-fatty livers (100%). In livers of obese mice (ob/ob), BPA sulfonation was lower (23%) than in livers from lean wild-type controls (100%). In addition to BPA sulfonation activity, Sult1a1 protein expression decreased by 97% in obese mouse livers.

conclusionTaken together these findings establish a profoundly reduced capacity of BPA elimination via sulfonation in obese or diabetic individuals and in those with fatty or cirrhotic livers versus individuals with healthy livers.

Indexed as

AnimalsBenzhydryl CompoundsBisphenol A CompoundsHumansLiver DiseasesMaleMetabolic DiseasesMiceMice, Inbred C57BLMice, KnockoutMice, ObesePhenolsSulfotransferasesBenzhydryl Compoundsbisphenol ABisphenol A CompoundsPhenolsSulfotransferasesBisphenol ACirrhosisDiabetesObesityPhase-IISteatosisSulfotransferase

Identifiers

PMID26712468
PMCPMC4724572
OpenAlexW2207432402

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.