Evidence map›Paper›PMID 24384915›Full record

ArticleDrug metabolism and disposition: the biological fate of chemicals2014

Modeling human nonalcoholic steatohepatitis-associated changes in drug transporter expression using experimental rodent models.

Mark J Canet, Rhiannon N Hardwick, April D Lake, Anika L Dzierlenga, John D Clarke, Nathan J Cherrington

Abstract read
In one paragraph

Article in Drug metabolism and disposition: the biological fate of chemicals, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–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

40 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Representative Rodent Models for Renal Transporter Alterations in Human Nonalcoholic Steatohepatitis.Drug metabolism and disposition: the biological fate of chemicals · 2023
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Nonalcoholic fatty liver disease alters microcystin-LR toxicokinetics and acute toxicity.Toxicon : official journal of the International Society on Toxinology · 2019
    Article
  19. Article
  20. Gene-by-Environment Interaction of BcrpDrug metabolism and disposition: the biological fate of chemicals · 2018
    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

6 authors.

Mark J CanetUniversity of Arizona, Department of Pharmacology and Toxicology, Tucson, Arizona.
Rhiannon N Hardwick
April D Lake
Anika L Dzierlenga
John D Clarke
Nathan J Cherrington

Funding

SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
Training in Environmental Toxicology of Human DiseaseT32ES007091 · NIEHS · UNIVERSITY OF ARIZONA · PI Nathan J Cherrington · 1985 to 2026
$10.7M
Pediatric Adverse Drug Reactions in NASHR01HD062489 · NICHD · UNIVERSITY OF ARIZONA · PI CHERRINGTON, NATHAN J · 2011 to 2015
$1.6M
Drug Transport at the Blood-Testis BarrierR01AI083927 · NIAID · UNIVERSITY OF ARIZONA · PI CHERRINGTON, NATHAN J · 2010 to 2013
$1.5M
NIAID NIH HHS AI083927NIAID NIH HHS R01 AI083927NICHD NIH HHS HD062489NICHD NIH HHS R01 HD062489NIEHS NIH HHS ES006694NIEHS NIH HHS ES007091NIEHS NIH HHS P30 ES006694NIEHS NIH HHS T32 ES007091
6 · The paper itself

Abstract

Nonalcoholic fatty liver disease is a prevalent form of chronic liver disease that can progress to the more advanced stage of nonalcoholic steatohepatitis (NASH). NASH has been shown to alter drug transporter regulation and may have implications in the development of adverse drug reactions. Several experimental rodent models have been proposed for the study of NASH, but no single model fully recapitulates all aspects of the human disease. The purpose of the current study was to determine which experimental NASH model best reflects the known alterations in human drug transporter expression to enable more accurate drug disposition predictions in NASH. Both rat and mouse NASH models were used in this investigation and include the methionine and choline deficient (MCD) diet model, atherogenic diet model, ob/ob and db/db mice, and fa/fa rats. Pathologic scoring evaluations demonstrated that MCD and atherogenic rats, as well as ob/ob and db/db mice, developed NASH. Liver mRNA and protein expression analyses of drug transporters showed that in general, efflux transporters were induced and uptake transporters were repressed in the rat MCD and the mouse ob/ob and db/db models. Lastly, concordance analyses suggest that both the mouse and rat MCD models as well as mouse ob/ob and db/db NASH models show the most similarity to human transporter mRNA and protein expression. These results suggest that the MCD rat and mouse model, as well as the ob/ob and db/db mouse models, may be useful for predicting altered disposition of drugs with similar kinetics across humans and rodents.

Indexed as

Disease Models, AnimalAnimalsCholine DeficiencyDiabetes Mellitus, ExperimentalDiet, AtherogenicFatty LiverMaleMethionineMiceMice, Inbred C57BLObesityOrganic Anion TransportersPharmaceutical PreparationsRatsRats, Sprague-DawleyTissue DistributionMethionineOrganic Anion TransportersPharmaceutical Preparations

Identifiers

PMID24384915
PMCPMC3965900

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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.