Evidence map›Paper›PMID 42327121›Full record

ArticlebioRxiv : the preprint server for biology2026

A membrane homeostatic response to lipid overload coordinates fatty acid metabolism.

Xiaojun Xiang, Yohannes A Ambaw, Ozlem Tok, Sheng Hui, Wei-Chun Tang, Arda Mizrak, Qingyue Zhang, Luke Cohen-Abeles, Robert V Farese, Tobias C Walther

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. 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

10 authors.

Xiaojun XiangCell Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID 0009-0008-8869-0443
Yohannes A AmbawCell Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Ozlem TokDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Sheng HuiDepartment of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Wei-Chun TangCell Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Arda MizrakCell Biology Department, Harvard Medical School, Boston, MA, USA.
Qingyue ZhangCell Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Luke Cohen-AbelesCell Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Robert V FareseCell Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Tobias C WaltherCell Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID 0000-0003-1442-1327

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Michael Jason de la Cruz · 1985 to 2026
$347.4M
Physiology of Lipid Droplets and Triglyceride StorageR01DK101579 · NIDDK · HARVARD SCHOOL OF PUBLIC HEALTH · PI FARESE, ROBERT V · 2014 to 2018
$2.6M
Lipid Droplets and Transcriptional Regulation of MetabolismR01DK124913 · NIDDK · SLOAN-KETTERING INST CAN RESEARCH · PI FARESE, ROBERT V, WALTHER, TOBIAS C · 2020 to 2024
$2.4M
Mechanisms of Lipid Droplet Protein TargetingR35GM158422 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI Tobias C Walther · 2025 to 2026
$880k
NCI NIH HHS P30 CA008748NIDDK NIH HHS R01 DK101579NIDDK NIH HHS R01 DK124913NIGMS NIH HHS R35 GM158422
6 · The paper itself

Abstract

Excess fatty acids can disrupt membrane and organelle function. Cells buffer fatty acid toxicity by synthesizing and storing triglycerides (TGs) in lipid droplets, but their capacity for TG storage is limited. Here, we impaired TG synthesis in hepatocytes and identified adaptive pathways that restore homeostasis during lipid overload. Transcription responds by activating fatty acid oxidation through peroxisome proliferator-activated receptors, and by suppressing synthesis of new, unsaturated fatty acids through sterol regulatory element-binding protein 1 (SREBP1). Mechanistically, SREBP1 appears to respond to changes in ER membrane fluidity. These findings reveal a homeostatic system monitoring and maintaining the ER membrane, coordinating fatty acid synthesis and oxidation, a finding with broad implications for understanding lipid physiology and developing TG synthesis inhibitors for treating fatty liver disease.

Indexed as

endoplasmic reticulumfatty acidhomeostasislipogenesismembrane fluiditySREBP1transcriptional responsetriglycerides

Identifiers

PMID42327121
PMCPMC13277988

What Socratic holds

Textmetadata
LicenceCC BY
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.