Evidence map›Paper›PMID 29417450›Full record

ReviewCurrent environmental health reports2018

Zebrafish as a Model for Toxicological Perturbation of Yolk and Nutrition in the Early Embryo.

Karilyn E Sant, Alicia R Timme-Laragy

Open access · greenAbstract readReview
In one paragraph

Review in Current environmental health reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
15.6field-weighted citation impact, top 1% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 172 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Antioxidants (Basel, Switzerland) · 2026
    Article
  6. Transient fetal hyperglycemia reprograms adipogenesis, lipogenesis, and insulin signaling in zebrafish.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Effects ofMolecules (Basel, Switzerland) · 2025
    Article
  14. Article
  15. Developmental perfluorooctanesulfonic acid exposure impairs exocrine pancreas function in zebrafish (Danio rerio).Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  16. Article
  17. Article
  18. 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

2 authors at 1 institution in 1 country.

Karilyn E SantDepartment of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts, Goessman 171, 686 N Pleasant St, Amherst, MA, 01003, USA.
Alicia R Timme-LaragyDepartment of Environmental Health Sciences, School of Public Health and Health Sciences, University of Massachusetts, Goessman 171, 686 N Pleasant St, Amherst, MA, 01003, USA. aliciat@umass.edu.
University of Massachusetts Amherst · US

Funding

Activation of Nrf2 during embryonic development: mechanisms and consequencesR01ES025748 · NIEHS · UNIVERSITY OF MASSACHUSETTS AMHERST · PI Alicia R Timme-Laragy · 2016 to 2026
$4.0M
Toxicant disruption of receptor-mediated endocytosis in oogenesis and later life metabolic dysfunctionR01ES028201 · NIEHS · UNIVERSITY OF MASSACHUSETTS AMHERST · PI TIMME-LARAGY, ALICIA R · 2017 to 2021
$2.1M
Interactions between PPAR, embryonic nutrition, and the developmental origins of metabolic dysfunctionF32ES028085 · NIEHS · UNIVERSITY OF MASSACHUSETTS AMHERST · PI SANT, KARILYN ELIZABETH · 2017 to 2018
$82k
NIEHS NIH HHS F32 ES028085NIEHS NIH HHS R01 ES025748NIEHS NIH HHS R01 ES028201
6 · The paper itself

Abstract

purpose of reviewDevelopmental toxicity assessments often focus on structural outcomes and overlook subtle metabolic differences which occur during the early embryonic period. Deviant embryonic nutrition can result in later-life disease, including diabetes, obesity, and cardiovascular disease. Prior to placenta-mediated nutrient exchange, the human embryo requires maternally supplied nutritional substrates for growth, called yolk. Here, we compare the biology of the human and zebrafish yolk and review examples of toxicant-mediated perturbation of yolk defects, composition, and utilization. RECENT

findingsZebrafish embryos, like human embryos, have a protruding yolk sac that serves as a nutritional cache. Aberrant yolk morphology is a common qualitative finding in fish embryotoxicity studies, but quantitative assessment and characterization provides an opportunity to uncover mechanistic targets of toxicant effects on embryonic nutrition. The zebrafish and the study of its yolk sac is an excellent model for uncovering toxicant disruptions to early embryonic nutrition and has potential to discover mechanistic insights into the developmental origins of health and disease.

Indexed as

Disease Models, AnimalAnimalsEgg YolkEmbryonic DevelopmentEmbryo, NonmammalianNutritional Physiological PhenomenaToxicologyZebrafishDevelopmental toxicologyEmbryonic nutritionMalabsorptionYolkYolk sac

Identifiers

PMID29417450
PMCPMC5876134
OpenAlexW2794224431

What OpenQuestion holds

Textmetadata
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.