ArticlebioRxiv : the preprint server for biology2026
A membrane homeostatic response to lipid overload coordinates fatty acid metabolism.
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.
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10 authors.
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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.
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