Evidence map›Paper›PMID 37230767›Full record

ArticleDrug metabolism and disposition: the biological fate of chemicals2023

Adipocyte-Derived PXR Signaling Is Dispensable for Diet-Induced Obesity and Metabolic Disorders in Mice.

Fang Wang, Jingwei Liu, Rebecca Hernandez, Se-Hyung Park, Ying-Jing Lai, Shuxia Wang, Bruce Blumberg, Changcheng Zhou

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Drug metabolism and disposition: the biological fate of chemicals, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Physiological Functions and Pathological Roles of PXR.Journal of the Endocrine Society · 2025
    Review
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

8 authors at 3 institutions in 1 country.

Fang WangDepartment of Pharmacology and Nutritional Sciences, College of Medicine, University of Kentucky, Lexington, Kentucky (F.W., S.-H.P., S.W.); Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California (J.L., R.H., Y.-J.L., C.Z.); and Department of Developmental and Cell Biology, School of Biological Sciences, University of California, Irvine, Irvine, California (B.B.).
Jingwei LiuDepartment of Pharmacology and Nutritional Sciences, College of Medicine, University of Kentucky, Lexington, Kentucky (F.W., S.-H.P., S.W.); Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California (J.L., R.H., Y.-J.L., C.Z.); and Department of Developmental and Cell Biology, School of Biological Sciences, University of California, Irvine, Irvine, California (B.B.).
Rebecca HernandezDepartment of Pharmacology and Nutritional Sciences, College of Medicine, University of Kentucky, Lexington, Kentucky (F.W., S.-H.P., S.W.); Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California (J.L., R.H., Y.-J.L., C.Z.); and Department of Developmental and Cell Biology, School of Biological Sciences, University of California, Irvine, Irvine, California (B.B.).
Se-Hyung ParkDepartment of Pharmacology and Nutritional Sciences, College of Medicine, University of Kentucky, Lexington, Kentucky (F.W., S.-H.P., S.W.); Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California (J.L., R.H., Y.-J.L., C.Z.); and Department of Developmental and Cell Biology, School of Biological Sciences, University of California, Irvine, Irvine, California (B.B.).
Ying-Jing LaiDepartment of Pharmacology and Nutritional Sciences, College of Medicine, University of Kentucky, Lexington, Kentucky (F.W., S.-H.P., S.W.); Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California (J.L., R.H., Y.-J.L., C.Z.); and Department of Developmental and Cell Biology, School of Biological Sciences, University of California, Irvine, Irvine, California (B.B.).
Shuxia WangDepartment of Pharmacology and Nutritional Sciences, College of Medicine, University of Kentucky, Lexington, Kentucky (F.W., S.-H.P., S.W.); Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California (J.L., R.H., Y.-J.L., C.Z.); and Department of Developmental and Cell Biology, School of Biological Sciences, University of California, Irvine, Irvine, California (B.B.).
Bruce BlumbergDepartment of Pharmacology and Nutritional Sciences, College of Medicine, University of Kentucky, Lexington, Kentucky (F.W., S.-H.P., S.W.); Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California (J.L., R.H., Y.-J.L., C.Z.); and Department of Developmental and Cell Biology, School of Biological Sciences, University of California, Irvine, Irvine, California (B.B.).
Changcheng ZhouDepartment of Pharmacology and Nutritional Sciences, College of Medicine, University of Kentucky, Lexington, Kentucky (F.W., S.-H.P., S.W.); Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California (J.L., R.H., Y.-J.L., C.Z.); and Department of Developmental and Cell Biology, School of Biological Sciences, University of California, Irvine, Irvine, California (B.B.) changcheng.zhou@ucr.edu.
University of California, Riverside · USUniversity of Kentucky · USUniversity of California, Irvine · US

Funding

WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI James Alexander Fitzpatrick · 2013 to 2026
$27.1M
Transgenerational obesity caused by ancestral exposure to obesogens in utero: changes in germline genomic architecture, roles of gonadal somatic cells, and metabolomic analysis of sexual dimorphismR01ES023316 · NIEHS · UNIVERSITY OF CALIFORNIA-IRVINE · PI BRUCE BLUMBERG, TOSHIHIRO SHIODA · 2013 to 2026
$8.3M
Pilot Projects ProgramP30GM127211 · NIGMS · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2018 to 2022
$5.7M
Research Training in Environmental ToxicologyT32ES018827 · NIEHS · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI Yinsheng Wang · 2010 to 2026
$5.3M
Role of PXR in EDC-induced cardiovascular diseaseR35ES035015 · NIEHS · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI Changcheng Zhou · 2023 to 2026
$3.4M
The role of signaling adaptor protein epsin in atherosclerosisR01HL156362 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, SHI, JINJUN · 2021 to 2024
$3.1M
The Role of Adaptor Protein Disabled-2 in Maintaining Endothelial Cell Function in AtherosclerosisR01HL162367 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, SHI, JINJUN · 2022 to 2025
$3.0M
Role of PXR in drug-elicited cardiovascular diseaseR01HL167206 · NHLBI · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI Hong Chen, Changcheng Zhou · 2023 to 2026
$2.8M
Endocrine disruptor mediated activation of PXR causes dyslipidemia and atherosclerosisR01ES023470 · NIEHS · UNIVERSITY OF KENTUCKY · PI ZHOU, CHANGCHENG · 2013 to 2022
$2.7M
Role of SMPDL3B in obesity-associated non-alcoholic fatty liver diseaseR01DK131786 · NIDDK · UNIVERSITY OF KENTUCKY · PI Shuxia Wang · 2022 to 2026
$2.5M
Interactions between prenatal obesogen exposure and Total Western diet lead to a transgenerational thrifty phenotype: functional and epigenomic analysis of effects in fat and liverR01ES031139 · NIEHS · UNIVERSITY OF CALIFORNIA-IRVINE · PI BLUMBERG, BRUCE, SHIODA, TOSHIHIRO · 2020 to 2025
$2.4M
Role of IKKβ in obesity and atherosclerosisR01HL131925 · NHLBI · UNIVERSITY OF KENTUCKY · PI ZHOU, CHANGCHENG · 2016 to 2019
$1.5M
BLRD VA I01 BX004252NHLBI NIH HHS R01 HL123358NHLBI NIH HHS R01 HL131925NHLBI NIH HHS R01 HL156362NHLBI NIH HHS R01 HL162367NHLBI NIH HHS R01 HL167206NIDDK NIH HHS P30 DK020579NIDDK NIH HHS R01 DK131786NIEHS NIH HHS R01 ES023316NIEHS NIH HHS R01 ES023470NIEHS NIH HHS R01 ES031139NIEHS NIH HHS R35 ES035015NIEHS NIH HHS T32 ES018827NIGMS NIH HHS P30 GM127211
6 · The paper itself

Abstract

Pregnane X receptor (PXR) is a xenobiotic receptor that can be activated by numerous chemicals including endogenous hormones, dietary steroids, pharmaceutical agents, and environmental chemicals. PXR has been established to function as a xenobiotic sensor to coordinately regulate xenobiotic metabolism by regulating the expression of many enzymes and transporters required for xenobiotic metabolism. Recent studies have implicated a potentially important role for PXR in obesity and metabolic disease beyond xenobiotic metabolism, but how PXR action in different tissues or cell types contributes to obesity and metabolic disorders remains elusive. To investigate the role of adipocyte PXR in obesity, we generated a novel adipocyte-specific PXR deficient mouse model (PXR

Indexed as

Insulin ResistanceReceptors, SteroidAdipocytesAnimalsDiet, High-FatMaleMiceObesityPregnane X ReceptorXenobioticsPregnane X ReceptorReceptors, SteroidXenobiotics

Identifiers

PMID37230767
PMCPMC10449100
OpenAlexW4378193809

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.