Evidence map›Paper›PMID 40737281›Full record

ArticleJournal of toxicology and environmental health. Part A2026

Does consumption of a high-fructose diet during pregnancy and lactation exacerbate the effects of maternal exposure to cadmium on development and metabolic function of mouse offspring?

Christopher Lau, Kaberi P Das, Joseph P Pancras, Lillian F Strader, Michael G Narotsky, Janice A Dye, Makala L Moore, Urmila P Kodavanti, Thomas W Jackson, Xuting Wang and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of toxicology and environmental health. Part A, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. The effects of cadmium and high fructose diet on metabolic and reproductive health in female CD-1 mice.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2025
    Article
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

20 authors.

Christopher LauPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment,Research Triangle Park, NC, USA.
Kaberi P DasPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment,Research Triangle Park, NC, USA.
Joseph P PancrasPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment,Research Triangle Park, NC, USA.
Lillian F StraderPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment,Research Triangle Park, NC, USA.
Michael G NarotskyPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment,Research Triangle Park, NC, USA.
Janice A DyePublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment,Research Triangle Park, NC, USA.
Makala L MooreOak Ridge Institute for Science and Education, U.S. Department of Energy, Oak Ridge, TN, USA.
Urmila P KodavantiPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment,Research Triangle Park, NC, USA.
Thomas W JacksonPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment,Research Triangle Park, NC, USA.ORCID 0000-0002-7996-0412
Xuting WangDivision of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Jian-Liang LiDivision of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Douglas A BellDivision of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Jennifer O'NeillOak Ridge Institute for Science and Education, U.S. Department of Energy, Oak Ridge, TN, USA.
Theodore A SlotkinDepartment of Pharmacology and Cancer Research, Duke University Medical Center, Durham, NC, USA.
Ivy GuyotteOak Ridge Institute for Science and Education, U.S. Department of Energy, Oak Ridge, TN, USA.
Gleta K CarswellChemical Characterization and Exposure Division, Center for Computational Toxicology and Exposure, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC, USA.
Jerry LiuChemical Characterization and Exposure Division, Center for Computational Toxicology and Exposure, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC, USA.
J Christopher CortonChemical Characterization and Exposure Division, Center for Computational Toxicology and Exposure, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC, USA.
Brian N ChorleyChemical Characterization and Exposure Division, Center for Computational Toxicology and Exposure, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC, USA.
Colette N MillerPublic Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment,Research Triangle Park, NC, USA.ORCID 0000-0001-7599-7886

Funding

Intramural NIH HHS Z99 ES999999
6 · The paper itself

Abstract

Exposures to pollutants rarely occur in isolation, often coexisting with other environmental stressors such as diet and may be particularly insidious in early life. The aim of this study was to examine effects of maternal exposure to cadmium (Cd) and consumption of a high-fructose diet (HFrD) on development of mouse offspring. Female CD-1 mice were administered either 0.5 or 5 ppm Cd in drinking water with or without an approximate 60% fructose diet for 3 weeks prior to mating. Dams were maintained on the same treatment until postnatal day (PND) 16. Cadmium concentrations in maternal, fetal, and neonatal liver increased in a concentration-dependent manner irrespective of diet. Endpoints known to be associated with Cd or HFrD adverse effects were assessed longitudinally in offspring from birth to young adulthood, including growth trajectory, pubertal development, body composition, glycemic tolerance and hepatic lipid accumulation. Maternal exposure to either Cd or HFrD alone significantly advanced onset of puberty, hypoglycemia, and reduced adiposity in adulthood. HFrD rarely exacerbated metal-initiated effects in most of the endpoints examined outside of pubertal timing. Because of chronic effects attributed to Cd or HFrD on metabolic function (e.g. glucose tolerance), transcriptomics and gene methylation analyses were performed on livers from neonatal and adult offspring. Data were largely consistent with phenotypic findings. In summary, maternal exposure to Cd or HFrD alone perturbed growth and development, producing long-lasting changes in metabolic function in adult offspring. HFrD did not appear to significantly exaggerate adverse outcomes attributed to metal exposure in the endpoints examined.

Indexed as

CadmiumEnvironmental PollutantsFructoseMaternal ExposurePrenatal Exposure Delayed EffectsAnimalsDietFemaleLactationLiverMaleMicePregnancyCadmiumEnvironmental PollutantsFructoseCadmiumdevelopmenthigh-fructose dietmetabolic functionmouse

Identifiers

PMID40737281
PMCPMC12440576

What Socratic 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 Socratic graph.