Evidence map›Paper›PMID 33004990›Full record

ArticleScientific reports2020

Intrauterine exposure to low-dose DBP in the mice induces obesity in offspring via suppression of UCP1 mediated ER stress.

Huan Li, Jianqiao Li, Zhenting Qu, Honghao Qian, Jing Zhang, Hongyan Wang, Xiaolei Xu, Shengyuan Liu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. A systematic review of exposure to endocrine disruptors and energy expenditure in mice.Environmental health : a global access science source · 2025
    Pooled it
  2. Article
  3. Prenatal exposure to environmentally relevant low-dosage dibutyl phthalate reduces placental efficiency in CD-1 mice.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Endocrine-Disrupting Chemicals and Disease Endpoints.International journal of molecular sciences · 2023
    Review
  8. Review
  9. Review
  10. Article
  11. 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.

Huan Li *School of Public Health, Beihua University, Jilin, 132013, China.
Jianqiao Li *School of Public Health, Beihua University, Jilin, 132013, China.
Zhenting QuJilin Combine Traditional Chinese and Western Hospital, Jilin, 132012, China.
Honghao QianSchool of Public Health, Beihua University, Jilin, 132013, China.
Jing ZhangSchool of Public Health, Beihua University, Jilin, 132013, China.
Hongyan WangSchool of Public Health, Beihua University, Jilin, 132013, China.
Xiaolei XuSchool of Public Health, Beihua University, Jilin, 132013, China.
Shengyuan LiuShenzhen Nanshan Center for Chronic Disease Control, Shenzhen, 518054, China. liushenglb@126.com.
Beihua University · CNJilin City Central Hospital · CNShenzhen Nanshan Center for Chronic Disease Control · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dibutyl phthalate (DBP) is recognized as an environmental endocrine disruptor that has been detected in fetal and postnatal samples. Recent evidence found that in utero DBP exposure was associated with an increase of adipose tissue weight and serum lipids in offspring, but the precise mechanism is unknown. Here we aimed to study the effects of in utero DBP exposure on obesity in offspring and examine possible mechanisms. SPF C57BL/6J pregnant mice were gavaged with either DBP (5 mg /kg/day) or corn oil, from gestational day 12 until postnatal day 7. After the offspring were weaned, the mice were fed a standard diet for 21 weeks, and in the last 2 weeks 20 mice were selected for TUDCA treatment. Intrauterine exposure to low-dose DBP promoted obesity in offspring, with evidence of glucose and lipid metabolic disorders and a decreased metabolic rate. Compared to controls, the DBP exposed mice had lower expression of UCP1 and significantly higher expression of Bip and Chop, known markers of endoplasmic reticulum (ER) stress. However, TUDCA treatment of DBP exposed mice returned these parameters nearly to the levels of the controls, with increased expression of UCP1, lower expression of Bip and Chop and ameliorated obesity. Intrauterine exposure of mice to low-dose DBP appears to promote obesity in offspring by inhibiting UCP1 via ER stress, a process that was largely reversed by treatment with TUDCA.

Indexed as

AnimalsApoptosisBody CompositionDibutyl PhthalateEndocrine DisruptorsEndoplasmic Reticulum StressEnergy MetabolismFemaleMiceObesityPregnancyPrenatal Exposure Delayed EffectsUncoupling Protein 1Dibutyl PhthalateEndocrine DisruptorsUncoupling Protein 1

Identifiers

PMID33004990
PMCPMC7529907
OpenAlexW3090213340

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.