Evidence map›Paper›PMID 29860300›Full record

ArticleEndocrinology2018

Retinoid X Receptor Activation During Adipogenesis of Female Mesenchymal Stem Cells Programs a Dysfunctional Adipocyte.

Bassem M Shoucri, Victor T Hung, Raquel Chamorro-García, Toshi Shioda, Bruce Blumberg

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
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  8. The Constituents ofScientifica · 2025
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  13. Triazole fungicides induce adipogenesis and repress osteoblastogenesis in zebrafish.Toxicological sciences : an official journal of the Society of Toxicology · 2023
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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

5 authors at 2 institutions in 1 country.

Bassem M ShoucriDepartment of Developmental and Cell Biology, University of California, Irvine, Irvine, California.
Victor T HungDepartment of Developmental and Cell Biology, University of California, Irvine, Irvine, California.
Raquel Chamorro-GarcíaDepartment of Developmental and Cell Biology, University of California, Irvine, Irvine, California.
Toshi ShiodaCenter for Cancer Research, Massachusetts General Hospital, Charlestown, Massachusetts.
Bruce BlumbergDepartment of Developmental and Cell Biology, University of California, Irvine, Irvine, California.
University of California, Irvine · USCenter for Cancer Research · US

Funding

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
Endocrine disrupter modulation of SXR in development and lymphomagenesisR01ES021832 · NIEHS · UNIVERSITY OF CALIFORNIA-IRVINE · PI BLUMBERG, BRUCE · 2013 to 2017
$1.9M
NIEHS NIH HHS R01 ES021832NIEHS NIH HHS R01 ES023316
6 · The paper itself

Abstract

Early life exposure to endocrine-disrupting chemicals (EDCs) is an emerging risk factor for the development of obesity and diabetes later in life. We previously showed that prenatal exposure to the EDC tributyltin (TBT) results in increased adiposity in the offspring. These effects linger into adulthood and are propagated through successive generations. TBT activates two nuclear receptors, the peroxisome proliferator-activated receptor (PPAR) γ and its heterodimeric partner retinoid X receptor (RXR), that promote adipogenesis in vivo and in vitro. We recently employed a mesenchymal stem cell (MSC) model to show that TBT promotes adipose lineage commitment by activating RXR, not PPARγ. This led us to consider the functional consequences of PPARγ vs RXR activation in developing adipocytes. We used a transcriptomal approach to characterize genome-wide differences in MSCs differentiated with the PPARγ agonist rosiglitazone (ROSI) or TBT. Pathway analysis suggested functional deficits in TBT-treated cells. We then compared adipocytes differentiated with ROSI, TBT, or a pure RXR agonist IRX4204 (4204). Our data show that RXR activators ("rexinoids," 4204 and TBT) attenuate glucose uptake, blunt expression of the antidiabetic hormone adiponectin, and fail to downregulate proinflammatory and profibrotic transcripts, as does ROSI. Finally, 4204 and TBT treatment results in an inability to induce markers of adipocyte browning, in part due to sustained interferon signaling. Taken together, these data implicate rexinoids in the development of dysfunctional white adipose tissue that could potentially exacerbate obesity and/or diabetes risk in vivo. These data warrant further screening and characterization of EDCs that activate RXR.

Indexed as

AdipocytesAdipogenesisAdipose Tissue, WhiteAnimalsCell DifferentiationCyclopropanesEndocrine DisruptorsFemaleHypoglycemic AgentsMesenchymal Stem CellsMicePPAR gammaRetinoid X ReceptorsRosiglitazoneTrialkyltin CompoundsCyclopropanesEndocrine DisruptorsHypoglycemic AgentsIRX4204PPAR gammaRetinoid X ReceptorsRosiglitazoneTrialkyltin Compoundstributyltin

Identifiers

PMID29860300
PMCPMC6669823
OpenAlexW2807127529

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.