Evidence map›Paper›PMID 39865409›Full record

ArticleLiver international : official journal of the International Association for the Study of the Liver2025

Maternal Western Diet Programmes Bile Acid Dysregulation and Hepatic Fibrosis in Fetal and Juvenile Macaques.

Michael J Nash, Evgenia Dobrinskikh, Saif I Al-Juboori, Rachel C Janssen, Jolyn Fernandes, Amy Argabright, Angelo D'Alessandro, Melissa A Kirigiti, Paul Kievit, Kjersti M Aagaard and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Liver international : official journal of the International Association for the Study of the Liver, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

16 authors.

Michael J NashDepartment of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.ORCID 0000-0002-4390-4531
Evgenia DobrinskikhDepartment of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
Saif I Al-JubooriDepartment of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
Rachel C JanssenHarold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.ORCID 0000-0001-7893-4848
Jolyn FernandesDepartment of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Amy ArgabrightDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
Angelo D'AlessandroDepartment of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
Melissa A KirigitiDivision of Cardiometabolic Health, Oregon Health Science University, Oregon National Primate Research Center, Beaverton, Oregon, USA.
Paul KievitDivision of Cardiometabolic Health, Oregon Health Science University, Oregon National Primate Research Center, Beaverton, Oregon, USA.
Kjersti M AagaardDepartment of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, Baylor College of Medicine, Houston, Texas, USA.
Carrie E McCurdyDepartment of Human Physiology, University of Oregon, Eugene, Oregon, USA.
Maureen GannonDepartment of Medicine, Division of Diabetes, Endocrinology, and Metabolism, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Kenneth L JonesHarold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Tiangang LiHarold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Jacob E FriedmanHarold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.ORCID 0000-0002-6426-1512
Stephanie R WesolowskiDepartment of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.ORCID 0000-0001-7523-0394

Funding

PILOT STUDY--SUBSTRATE METABOLISM IN EXTREMELY LOW BIRTH WEIGHT INFANTSP30DK048520 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI BRYAN C BERGMAN · 1995 to 2026
$32.6M
Metformin in Pregnancy: Fetal Consequences & Long-term Offspring Outcomes in a NHP ModelR01DK128187 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI FRIEDMAN, JACOB E, KIEVIT, PAUL · 2021 to 2025
$7.3M
Regulation of Bile Acid Metabolism and Signaling in Metabolic DiseasesR01DK117965 · NIDDK · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Tiangang Li · 2019 to 2026
$2.7M
Sulfur Amino Acid Metabolism and Regulation of Hepatic Metabolic FlexibilityR01DK131064 · NIDDK · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI LI, TIANGANG · 2022 to 2025
$1.6M
Novel Roles of Cullin-RING E3 Ligases in Liver PathophysiologyR01DK134316 · NIDDK · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Tiangang Li · 2023 to 2026
$1.5M
MECHANISMS FOR FETAL HEPATIC PROGRAMMING IN THE NON-HUMAN PRIMATE (NHP)R01DK078590 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI FRIEDMAN, JACOB E · 2007 to 2010
$1.5M
NIDDK NIH HHS P30 DK048520NIDDK NIH HHS R01 DK078590NIDDK NIH HHS R01 DK117965NIDDK NIH HHS R01 DK128187NIDDK NIH HHS R01 DK131064NIDDK NIH HHS R01 DK134316NIH Office of the DirectorNINDS NIH HHS
6 · The paper itself

Abstract

BACKGROUND AND

aimsMaternal obesity increases the risk of the paediatric form of metabolic dysfunction-associated steatotic liver disease (MASLD), affecting up to 30% of youth, but the developmental origins remain poorly understood.

methodsUsing a Japanese macaque model, we investigated the impact of maternal Western-style diet (mWSD) or chow diet followed by postweaning WSD (pwWSD) or chow diet focusing on bile acid (BA) homeostasis and hepatic fibrosis in livers from third-trimester fetuses and 3-year-old juvenile offspring.

resultsJuveniles exposed to mWSD had increased hepatic collagen I/III content and stellate cell activation in portal regions. mWSD increased transcriptional signatures of FXR activation, while pwWSD impaired FXR pathway genes and increased liver BA content. Both mWSD and pwWSD increased serum BA concentrations. Notably, mWSD-exposed juvenile offspring had increased periportal CK19 expression and cholangiocyte gene expression supporting proliferation compared with maternal chow-exposed offspring. Fetuses exposed to mWSD had increased CK19 expression and hepatic BAs which correlated positively with periportal collagen deposition and negatively with markers of fetal oxygenation. In juvenile offspring, increased serum BAs correlated positively with hepatic oxidative stress and portal fibrosis without elevated liver enzymes.

conclusionsmWSD is associated with hallmarks of paediatric MASLD including portal bile ductular reaction, portal fibrosis and dysregulated BA homeostasis. These conditions begin in utero and persist in juvenile offspring regardless of their postweaning diet. These findings implicate changes in BA metabolism that may drive developmental programming of MASLD in juvenile offspring beginning in utero.

Indexed as

Bile Acids and SaltsDiet, WesternLiver CirrhosisPrenatal Exposure Delayed EffectsAnimalsDisease Models, AnimalFemaleLiverMaleMaternal Nutritional Physiological PhenomenaPregnancyReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearBile Acids and SaltsReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and Nuclearcholestasisdevelopmental programmingFarnesoid X receptorliverPaediatric MASLDstellate cells

Identifiers

PMID39865409
PMCPMC11771692

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.