Evidence map›Paper›PMID 40208790›Full record

ArticleCell reports2025

Dietary oleic acid drives obesogenic adipogenesis via modulation of LXRα signaling.

Allison Wing, Elise Jeffery, Christopher D Church, Jennifer Goodell, Rocío Del M Saavedra-Peña, Moumita Saha, Brandon Holtrup, Maud Voisin, N Sima Alavi, Mariana Floody and 6 more

Abstract read
In one paragraph

Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
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  8. 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.

Allison WingDepartment of Molecular, Cell, and Developmental Biology, Yale University, 219 Prospect St., New Haven, CT 06520, USA.
Elise JefferyDepartment of Cell Biology, Yale University School of Medicine, 333 Cedar St., New Haven, CT 06520, USA.
Christopher D ChurchDepartment of Comparative Medicine, Yale University School of Medicine, 310 Cedar St., New Haven, CT 06520, USA.
Jennifer GoodellDepartment of Comparative Medicine, Yale University School of Medicine, 310 Cedar St., New Haven, CT 06520, USA.
Rocío Del M Saavedra-PeñaDepartment of Molecular, Cell, and Developmental Biology, Yale University, 219 Prospect St., New Haven, CT 06520, USA.
Moumita SahaDepartment of Comparative Medicine, Yale University School of Medicine, 310 Cedar St., New Haven, CT 06520, USA.
Brandon HoltrupDepartment of Molecular, Cell, and Developmental Biology, Yale University, 219 Prospect St., New Haven, CT 06520, USA.
Maud VoisinDepartment of Microbiology, NYU School of Medicine, New York, NY 10016, USA.
N Sima AlaviDepartment of Comparative Medicine, Yale University School of Medicine, 310 Cedar St., New Haven, CT 06520, USA.
Mariana FloodyDepartment of Comparative Medicine, Yale University School of Medicine, 310 Cedar St., New Haven, CT 06520, USA.
Zenan WangDepartment of Molecular, Cell, and Developmental Biology, Yale University, 219 Prospect St., New Haven, CT 06520, USA.
Thomas E ZapadkaDepartment of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Michael J GarabedianDepartment of Microbiology, NYU School of Medicine, New York, NY 10016, USA; Department of Medicine, NYU School of Medicine, New York, NY 10016, USA.
Rohan VarshneyDepartment of Biochemistry and Physiology and Harold Hamm Diabetes Center, Oklahoma University Health Sciences, Oklahoma City, OK 73104, USA.
Michael C RudolphDepartment of Biochemistry and Physiology and Harold Hamm Diabetes Center, Oklahoma University Health Sciences, Oklahoma City, OK 73104, USA. Electronic address: michael-rudolph@ouhsc.edu.
Matthew S RodehefferDepartment of Molecular, Cell, and Developmental Biology, Yale University, 219 Prospect St., New Haven, CT 06520, USA; Department of Cell Biology, Yale University School of Medicine, 333 Cedar St., New Haven, CT 06520, USA; Yale Stem Cell Center, Yale University School of Medicine, 10 Amistad St., New Haven, CT 06520, USA; Yale Center of Molecular and Systems Metabolism, Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address: matthew.rodeheffer@yale.edu.

Funding

Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI Eric P. Winer · 1985 to 2026
$85.0M
Cellular & molecular mechanisms of white adipose tissue mass regulationR01DK090489 · NIDDK · YALE UNIVERSITY · PI RODEHEFFER, MATTHEW S · 2011 to 2020
$3.8M
The role of mitochondrial dynamics in diet-influenced regulation of food intake and adiposityR01DK126447 · NIDDK · YALE UNIVERSITY · PI HORVATH, TAMAS L, RODEHEFFER, MATTHEW S · 2021 to 2024
$2.3M
Defining the role of an endothelial-adipocyte precursor axis in adipocyte hyperplasiaR01DK132563 · NIDDK · YALE UNIVERSITY · PI Matthew S Rodeheffer · 2023 to 2026
$2.2M
Dietary regulation of adipocyte hyperplasia in obesity: Impact on adipose mass and metabolic diseaseR01DK110147 · NIDDK · YALE UNIVERSITY · PI RODEHEFFER, MATTHEW S · 2016 to 2019
$1.9M
High Performance Computing Instrumentation for the Yale Center for Genome AnalysisS10OD030363 · OD · YALE UNIVERSITY · PI MANE, SHRIKANT M · 2022 to 2022
$1.2M
Flow cytometer for high-parameter analysesS10OD026996 · OD · YALE UNIVERSITY · PI HABERMAN, ANN M · 2019 to 2019
$596k
Cellular and molecular mechanisms of white adipose tissue regulation in development and diseaseR56DK090489 · NIDDK · YALE UNIVERSITY · PI RODEHEFFER, MATTHEW S · 2016 to 2016
$209k
Retinal Circuitry Response to Nerve InjuryF31EY034776 · NEI · YALE UNIVERSITY · PI ZAPADKA, THOMAS EUGENE · 2023 to 2025
$146k
NCI NIH HHS P30 CA016359NEI NIH HHS F31 EY034776NIDDK NIH HHS R01 DK090489NIDDK NIH HHS R01 DK110147NIDDK NIH HHS R01 DK126447NIDDK NIH HHS R01 DK132563NIDDK NIH HHS R56 DK090489NIH HHS S10 OD026996NIH HHS S10 OD030363
6 · The paper itself

Abstract

Dietary fat composition has changed substantially during the obesity epidemic. As adipocyte hyperplasia is a major mechanism of adipose expansion, we aim to ascertain how dietary fats affect adipogenesis during obesity. We employ an unbiased dietary screen to identify oleic acid (OA) as the only dietary fatty acid that induces obesogenic hyperplasia at physiologic levels and show that plasma monounsaturated fatty acids (MUFAs), which are mostly OA, are associated with human obesity. OA stimulates adipogenesis in mouse and human adipocyte precursor cells (APCs) by increasing AKT2 signaling, a hallmark of obesogenic hyperplasia, and reducing LXR activity. High OA consumption decreases LXRα Ser196 phosphorylation in APCs, while blocking LXRα phosphorylation results in APC hyperproliferation. As OA is increasingly being incorporated into dietary fats due to purported health benefits, our finding that OA is a unique physiologic regulator of adipose biology underscores the importance of understanding how high OA consumption affects metabolic health.

Indexed as

AdipogenesisDietary FatsLiver X ReceptorsObesityOleic AcidSignal Transduction3T3-L1 CellsAdipocytesAnimalsHumansMaleMiceMice, Inbred C57BLPhosphorylationProto-Oncogene Proteins c-aktDietary FatsLiver X ReceptorsOleic AcidProto-Oncogene Proteins c-aktadipocyte stem celladipogenesisCP: MetabolismLXRobesityoleic acid

Identifiers

PMID40208790
PMCPMC12073628

What OpenQuestion holds

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Read underepoch 390

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.