Evidence map›Paper›PMID 40305361›Full record

ArticleBiomolecules2025

Docosahexaenoic Acid Supplementation in Postnatal Growth Restricted Rats Does Not Normalize Lung Function or PPARγ Activity.

Adrienne J Cohen, Wesley R Chidester, Daniel T Wray, Nicolette Jessen, Aimee Jones, Cheylah Bitsui, James Zhao, J Alan Maschek, James E Cox, Camilia R Martin and 1 more

Abstract read
In one paragraph

Article in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Adrienne J CohenDepartment of Pediatrics, University of Utah, Salt Lake City, UT 84108, USA.
Wesley R ChidesterDepartment of Pediatrics, University of Utah, Salt Lake City, UT 84108, USA.
Daniel T WrayDepartment of Pediatrics, University of Utah, Salt Lake City, UT 84108, USA.
Nicolette JessenDepartment of Pediatrics, University of Utah, Salt Lake City, UT 84108, USA.
Aimee JonesDepartment of Pediatrics, University of Utah, Salt Lake City, UT 84108, USA.
Cheylah BitsuiDepartment of Pediatrics, University of Utah, Salt Lake City, UT 84108, USA.
James ZhaoDepartment of Pediatrics, University of Utah, Salt Lake City, UT 84108, USA.
J Alan MaschekHealth Science Center Cores, University of Utah Health Sciences Center, Salt Lake City, UT 84108, USA.ORCID 0000-0003-3217-2299
James E CoxHealth Science Center Cores, University of Utah Health Sciences Center, Salt Lake City, UT 84108, USA.ORCID 0000-0002-5977-2350
Camilia R MartinDivision of Neonatology, Weill Cornell Medicine, New York, NY 10065, USA.
Lisa A Joss-MooreDepartment of Pediatrics, University of Utah, Salt Lake City, UT 84108, USA.ORCID 0000-0001-6820-0605

Funding

The Native American Short-Term Research Education Program in Children's Health Supplemental Proposal for additional Exceptional Mentoring ExperiencesR25HL108828 · NHLBI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI HOLSTI, MAIJA · 2011 to 2025
$1.6M
NIH HHS 1-S10-OD021505-01NIH HHS DK084036NIH HHS R25HL108828
6 · The paper itself

Abstract

The development of BPD in preterm neonates is increased by poor growth and nutritional deficits. The involvement of the fatty acid DHA in the development of BPD has been a focus for over a decade. However, recent clinical trials show that isolated DHA supplementation may increase BPD in subgroups of preterm neonates. One explanation for poor lung outcomes in DHA-supplemented neonates is a disruption of global fatty acid profiles and increased expression of a dominant-negative splice variant of a key driver of lung development, PPARγ. We previously developed a rat model of postnatal growth restriction (PGR) in which pups have impaired lung function and altered PPARγ activity. Here, we use our PGR rat model to assess the effects of DHA supplementation on lung outcomes. We hypothesize that the PPARγ splice variant, PPARγΔ5, will be expressed in the rat lung, and that DHA supplementation of PGR rat pups will alter circulating lipid profiles, lung mechanics, and PPARγ variant expression. Our findings demonstrate that PPARγΔ5 is expressed in the developing rat lung and that DHA supplementation of PGR rat pups alters global circulating fatty-acid profiles and does not normalize PGR-induced impaired lung mechanics or PPARγ activity.

Indexed as

Dietary SupplementsDocosahexaenoic AcidsLungPPAR gammaAnimalsAnimals, NewbornDisease Models, AnimalFemaleMaleRatsRats, Sprague-DawleyDocosahexaenoic AcidsPPAR gammaalternative splicingbronchopulmonary dysplasiaDHAgrowth restrictionlung developmentPPARγ

Identifiers

PMID40305361
PMCPMC12024927

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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.