Evidence map›Paper›PMID 25488932›Full record

ArticleDrug metabolism and disposition: the biological fate of chemicals2015

Renal xenobiotic transporter expression is altered in multiple experimental models of nonalcoholic steatohepatitis.

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

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Drug metabolism and disposition: the biological fate of chemicals, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Trial
  2. Article
  3. Western diet exacerbates a murine model of Balkan nephropathy.American journal of physiology. Renal physiology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. 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

7 authors at 2 institutions in 1 country.

Mark J CanetUniversity of Arizona, Department of Pharmacology and Toxicology, Tucson, Arizona (M.J.C., R.N.H., A.D.L., A.L.D., J.D.C., N.J.C.); and Rutgers University, Office of Translational Science, New Brunswick, New Jersey (M.J.G.).
Rhiannon N HardwickUniversity of Arizona, Department of Pharmacology and Toxicology, Tucson, Arizona (M.J.C., R.N.H., A.D.L., A.L.D., J.D.C., N.J.C.); and Rutgers University, Office of Translational Science, New Brunswick, New Jersey (M.J.G.).
April D LakeUniversity of Arizona, Department of Pharmacology and Toxicology, Tucson, Arizona (M.J.C., R.N.H., A.D.L., A.L.D., J.D.C., N.J.C.); and Rutgers University, Office of Translational Science, New Brunswick, New Jersey (M.J.G.).
Anika L DzierlengaUniversity of Arizona, Department of Pharmacology and Toxicology, Tucson, Arizona (M.J.C., R.N.H., A.D.L., A.L.D., J.D.C., N.J.C.); and Rutgers University, Office of Translational Science, New Brunswick, New Jersey (M.J.G.).
John D ClarkeUniversity of Arizona, Department of Pharmacology and Toxicology, Tucson, Arizona (M.J.C., R.N.H., A.D.L., A.L.D., J.D.C., N.J.C.); and Rutgers University, Office of Translational Science, New Brunswick, New Jersey (M.J.G.).
Michael J GoedkenUniversity of Arizona, Department of Pharmacology and Toxicology, Tucson, Arizona (M.J.C., R.N.H., A.D.L., A.L.D., J.D.C., N.J.C.); and Rutgers University, Office of Translational Science, New Brunswick, New Jersey (M.J.G.).
Nathan J CherringtonUniversity of Arizona, Department of Pharmacology and Toxicology, Tucson, Arizona (M.J.C., R.N.H., A.D.L., A.L.D., J.D.C., N.J.C.); and Rutgers University, Office of Translational Science, New Brunswick, New Jersey (M.J.G.) cherrington@pharmacy.arizona.edu.
University of Arizona · USRutgers, The State University of New Jersey · US

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 R01 AI083927NIAID NIH HHS R01-AI083927NICHD NIH HHS R01 HD062489NICHD NIH HHS R01-HD062489NIEHS NIH HHS ES007091NIEHS NIH HHS P30 ES006694NIEHS NIH HHS P30-ES006694NIEHS NIH HHS T32 ES007091
6 · The paper itself

Abstract

Nonalcoholic fatty liver disease is the most common chronic liver disease, which can progress to nonalcoholic steatohepatitis (NASH). Previous investigations demonstrated alterations in the expression and activity of hepatic drug transporters in NASH. Moreover, studies using rodent models of cholestasis suggest that compensatory changes in kidney transporter expression occur to facilitate renal excretion during states of hepatic stress; however, little information is currently known regarding extrahepatic regulation of drug transporters in NASH. The purpose of the current study was to investigate the possibility of renal drug transporter regulation in NASH across multiple experimental rodent models. Both rat and mouse NASH models were used in this investigation and include: the methionine and choline-deficient (MCD) diet, atherogenic diet, fa/fa rat, ob/ob and db/db mice. Histologic and pathologic evaluations confirmed that the MCD and atherogenic rats as well as the ob/ob and db/db mice all developed NASH. In contrast, the fa/fa rats did not develop NASH but did develop extensive renal injury compared with the other models. Renal mRNA and protein analyses of xenobiotic transporters suggest that compensatory changes occur in NASH to favor increased xenobiotic secretion. Specifically, both apical efflux and basolateral uptake transporters are induced, whereas apical uptake transporter expression is repressed. These results suggest that NASH may alter the expression and potentially function of renal drug transporters, thereby impacting drug elimination mechanisms in the kidney.

Indexed as

Disease Models, AnimalGene Expression RegulationAnimalsATP-Binding Cassette, Sub-Family C ProteinsATP Binding Cassette Transporter, Subfamily BGene Expression ProfilingKidneyLiverMaleMice, Inbred C57BLMice, Mutant StrainsNon-alcoholic Fatty Liver DiseaseOrganic Anion Transporters, Sodium-IndependentOrganic Cation Transport ProteinsProtein IsoformsRats, Mutant StrainsATP-Binding Cassette, Sub-Family C ProteinsATP Binding Cassette Transporter, Subfamily BOrganic Anion Transporters, Sodium-IndependentOrganic Cation Transport ProteinsProtein IsoformsRNA, Messenger

Identifiers

PMID25488932
PMCPMC4293398
OpenAlexW2100888886

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.