Evidence map›Paper›PMID 24980262›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2014

Human hepatic UGT2B15 developmental expression.

Karthika Divakaran, Ronald N Hines, D Gail McCarver

Open access · greenAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.6field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Ontogeny of Drug-Metabolizing Enzymes.Methods in molecular biology (Clifton, N.J.) · 2021
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Xenobiotic Metabolism in Mice Lacking the UDP-Glucuronosyltransferase 2 Family.Drug metabolism and disposition: the biological fate of chemicals · 2015
    Article
  17. Article
  18. 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

3 authors at 1 institution in 1 country.

Karthika DivakaranDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin kdivakar@mcw.edu.
Ronald N HinesDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin kdivakar@mcw.edu.
D Gail McCarverDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin.
Medical College of Wisconsin · US

Funding

Factors Determining Bisphenol A Disposition in Human InfantsR01ES017764 · NIEHS · MEDICAL COLLEGE OF WISCONSIN · PI MCCARVER, D GAIL · 2010 to 2013
$1.8M
NIEHS NIH HHS 5R01ES017764
6 · The paper itself

Abstract

Human hepatic UGT2B15 developmental expression changes may alter the metabolism of important drugs and toxicants such as bisphenol A (BPA). Previously, UGT2B15 ontogeny knowledge consisted of transcript data, a dubious surrogate for protein expression. Herein, UGT2B15 protein content was determined in human hepatic microsomes (n = 236, 8 weeks gestation to 18 years). The impact of a common, functional single nucleotide polymorphism (g.253G>T), present in UGT2B15*2 and *5 alleles, was also tested. UGT2B15 expression began during late fetal life, at about 18% of mature values (medians = 48, 267 pmoles/mg of microsomal protein, respectively; p < 0.001). UGT2B15 neonatal (n = 39) and late fetal (≥28 weeks, n = 10) content was similar, but lower than that of infants between 3 and 15 weeks age (n = 46; medians = 38, 48, 404 pmoles/mg microsomal protein, respectively; p < 0.001). Values for the latter group were higher compared with the remaining age group (15 weeks to 18 years; n = 82, p < 0.001). UGT2B15 expression varied 31-fold across the entire sample, and within groups, ranged from 4- to 27-fold. Among postnatal samples, age group, the presence of g.253T and male gender were each significantly associated with greater UGT2B15 expression (p < 0.001, <0.01, and <0.05, respectively; stepwise linear regression). In summary, hepatic UGT2B15 protein onset begins in late gestation; however, the greatest rate of change occurs during the first few weeks after birth. We speculate that the fetus and neonate may have lower clearance of some UGT2B15 substrates, such as BPA, compared with older individuals.

Indexed as

Gene Expression Regulation, DevelopmentalOrganogenesisAdolescentChildChild, PreschoolFemaleGestational AgeGlucuronosyltransferaseHumansInfantInfant, NewbornLiverMaleMicrosomes, LiverPolymorphism, Single NucleotidePregnancyGlucuronosyltransferaseUDP-glucuronosyltransferase 2B15, humanhepatic liver microsomesontogenysingle nucleotide polymorphismSNPUGTuridine diphosphate glucuronosyltransferase

Identifiers

PMID24980262
PMCPMC4271124
OpenAlexW2063279749

What OpenQuestion holds

Textmetadata
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.