Evidence map›Paper›PMID 40595890›Full record

ArticleScientific reports2025

Sexually dimorphic impact of prenatal hyperandrogenism on offspring growth trajectory in sheep.

Eylem Topaktas, Joseph Ciarelli, Stephanie Domke, Brooke Pallas, Adel Ghnenis, Mansi Agarwal, Charles Goss, Kevin Cho, Leah P Shriver, Gary J Patti and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. 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. 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

12 authors.

Eylem TopaktasDepartment of Pediatrics, Washington University St. Louis, St. Louis, MO, 63110, USA.
Joseph CiarelliDepartment of Pediatrics, University of Michigan, Ann Arbor, MI, USA.
Stephanie DomkeDepartment of Pediatrics, University of Michigan, Ann Arbor, MI, USA.
Brooke PallasUnit for Laboratory Animal Medicine, University of Michigan, Ann Arbor, MI, USA.
Adel GhnenisDepartment of Pediatrics, University of Michigan, Ann Arbor, MI, USA.
Mansi AgarwalCenter for Biostatistics and Data Science, Washington University, St Louis, MO, USA.
Charles GossCenter for Biostatistics and Data Science, Washington University, St Louis, MO, USA.
Kevin ChoCenter for Mass Spectrometry and Metabolic Tracing, Department of Chemistry, Department of Medicine, Washington University in St. Louis, St. Louis, MO, USA.
Leah P ShriverCenter for Mass Spectrometry and Metabolic Tracing, Department of Chemistry, Department of Medicine, Washington University in St. Louis, St. Louis, MO, USA.
Gary J PattiCenter for Mass Spectrometry and Metabolic Tracing, Department of Chemistry, Department of Medicine, Washington University in St. Louis, St. Louis, MO, USA.
Vasantha PadmanabhanDepartment of Pediatrics, University of Michigan, Ann Arbor, MI, USA.
Arpita Kalla VyasDepartment of Pediatrics, Washington University St. Louis, St. Louis, MO, 63110, USA. vyas@wustl.edu.

Funding

Gestational Hyperandrogenism in Cardiovascular ProgrammingR01HL139639 · NHLBI · WASHINGTON UNIVERSITY · PI PADMANABHAN, VASANTHA, VYAS, ARPITA · 2020 to 2023
$2.7M
Assessment of Placental Blood Volume Flow and Function in IUGR Using a Transfer Function ModelR21HD095501 · NICHD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RUBIN, JONATHAN M · 2019 to 2020
$448k
NHLBI NIH HHS HL139639NHLBI NIH HHS R01 HL139639NICHD NIH HHS R21 HD095501
6 · The paper itself

Abstract

In a translationally relevant ovine model of gestational hyperandrogenism we have previously reported cardiometabolic disruption in female offspring (males were not extensively studied). We hypothesized that gestational hyperandrogenism would lead to sex-specific disruption in offspring's growth, cytokine and metabolic milieu, potential mediators of cardiometabolic disease (CMD). 100 mg Testosterone propionate (T) or vehicle (C) was administered intramuscularly twice weekly between gestational days (GD) 30-90. Two cohorts of offspring were generated, including both males and females. Fetal weight and systemic metabolomics were analyzed in the fetal cohort (GD120). Growth trajectory, systemic cytokines, and metabolomics were analyzed in the postnatal cohort. Data was analyzed using mixed model ANOVA, student T-test, and Cohen D (d) analysis. T excess led to (1) a reduction in fetal weight at GD 120 in both sexes and sex-specific perturbations in the fetal metabolome, (2) T-Female had a growth trajectory similar to males and significantly different from C-Females (age x treatment interaction p = 0.028) and (3) sex-specific alterations in cytokine milieu at birth and metabolome in the pre-pubertal period. Altered sex-specific postnatal metabolic milieu and growth trajectory, notable for catch-up growth in T-Female, could have implications for sex-specific impact on the cardiometabolic function in the lambs.

Indexed as

HyperandrogenismPrenatal Exposure Delayed EffectsSex CharacteristicsAnimalsCytokinesFemaleFetal WeightMaleMetabolomeMetabolomicsPregnancySheepTestosterone PropionateCytokinesTestosterone PropionateGrowthOvinePrenatal testosterone excess

Identifiers

PMID40595890
PMCPMC12215409

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Registered trials

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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.