Evidence map›Paper›PMID 30660623›Full record

ArticleToxicology2019

In utero exposure to di(2-ethylhexyl)phthalate suppresses blood glucose and leptin levels in the offspring of wild-type mice.

Yumi Hayashi, Yuki Ito, Hisao Naito, Hazuki Tamada, Nozomi Yamagishi, Takaaki Kondo, Tetsuya Ishikawa, Frank J Gonzalez, Tamie Nakajima

Abstract read
In one paragraph

Article in Toxicology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

  1. Phthalates toxicityHeliyon · 2025
    Article
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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

9 authors at 5 institutions in 2 countries.

Yumi HayashiPathophysiological Laboratory Sciences, Department of Radiological and Medical Laboratory Sciences, Nagoya University Graduate School of Medicine, 1-1-20 Daiko-Minami, Higashi-ku, Nagoya, 461-8673, Japan; In vivo Real-time Omics Laboratory, Institute for Advanced Research, Nagoya University, Furo-cho, Chikusa-ku, Nagoya, 464-8601, Japan. Electronic address: yhayashi@met.nagoya-u.ac.jp.
Yuki ItoDepartment of Occupational and Environmental Health, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, 467-8601, Japan. Electronic address: yukey@med.nagoya-cu.ac.jp.
Hisao NaitoDepartment of Public Health, Fujita Health University School of Medicine, Dengakugakubo 1-98, Kutsukake-cho, Toyoake, 470-1192, Japan. Electronic address: naitoh@med.nagoya-u.ac.jp.
Hazuki TamadaDepartment of Occupational and Environmental Health, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan. Electronic address: tamada@kinjo-u.ac.jp.
Nozomi YamagishiDepartment of Occupational and Environmental Health, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan. Electronic address: yamagishi-nozomi-r@pref.nagano.lg.jp.
Takaaki KondoPathophysiological Laboratory Sciences, Department of Radiological and Medical Laboratory Sciences, Nagoya University Graduate School of Medicine, 1-1-20 Daiko-Minami, Higashi-ku, Nagoya, 461-8673, Japan. Electronic address: taka@met.nagoya-u.ac.jp.
Tetsuya IshikawaPathophysiological Laboratory Sciences, Department of Radiological and Medical Laboratory Sciences, Nagoya University Graduate School of Medicine, 1-1-20 Daiko-Minami, Higashi-ku, Nagoya, 461-8673, Japan. Electronic address: ishikawa@met.nagoya-u.ac.jp.
Frank J GonzalezLaboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: gonzalef@mail.nih.gov.
Tamie NakajimaCollege of Life and Health Sciences, Chubu University, 1200 Matsumoto-cho, Kasugai, Aichi, 487-8501, Japan. Electronic address: tnasu23@med.nagoya-u.ac.jp.
Nagoya City University · JPNagoya University · JPChubu University · JPFujita Health University Hospital · JPNational Institutes of Health · US

Funding

Xenobiotic receptorsZIABC005562 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 2009 to 2025
$26.9M
Xenobiotic ReceptorsZIABC005708 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 2009 to 2025
$16.4M
Intramural NIH HHS ZIA BC005562Intramural NIH HHS ZIA BC005708
6 · The paper itself

Abstract

Exposure of pregnant mice to di(2-ethylhexyl)phthalate (DEHP) induces maternal lipid malnutrition and decreases the number of live fetuses/pups. In this study, we aimed to clarify the relationship between maternal lipid malnutrition and the nutritional status of the neonatal, lactational, and adult offspring, as well as the role of peroxisome proliferator-activated receptor α (PPARα) in these relationships. Sv/129 wild-type (mPPARA), Ppara-null, and PPARα-humanized (hPPARA) mice were fed diets containing 0, 0.01, 0.05, or 0.1% DEHP in utero and/or during the lactational stage. The male offspring were killed on postnatal day 2 or 21, or after 11 weeks. Exposure to either 0.05% or 0.1% DEHP during both the in utero and lactational periods decreased serum glucose concentrations in 2-day-old mPPARA offspring. These dosages also decreased both serum and plasma leptin levels in both 2- and 21-day-old mPPARA offspring. In contrast, exposure to DEHP only during the lactational period did not decrease leptin levels, suggesting the importance of in utero exposure to DEHP. Exposure to 0.05% DEHP during the in utero and lactational periods also increased food consumption after weaning in both mPPARA and hPPARA mice; this was not observed in Ppara-null offspring. In conclusion, in utero exposure to DEHP induces neonatal serum glucose malnutrition via PPARα. DEHP also decreases serum and plasma leptin concentrations in offspring during the neonatal and weaning periods, in association with PPARα, which presumably results in increased of food consumption after weaning.

Indexed as

Maternal ExposurePrenatal Exposure Delayed EffectsAnimalsBlood GlucoseBody WeightCytochrome P450 Family 4Diethylhexyl PhthalateDose-Response Relationship, DrugFemaleLeptinMaleMiceMice, KnockoutOrgan SizePPAR alphaPregnancyBlood GlucoseCyp4a14 protein, mouseCytochrome P450 Family 4Diethylhexyl PhthalateLeptinPPAR alphaRNA, MessengerDEHPFeeding behaviorGlucoseIn utero exposureLeptinMalnutrition

Identifiers

PMID30660623
PMCPMC6628919
OpenAlexW2909036284

What OpenQuestion holds

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LicenceTDM
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.