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Peroxisome Proliferator-Activated Receptor α/δ/γ Activation Profile by Endogenous Long-Chain Fatty Acids.

Akihiro Honda¹, Aoi Hosoda¹, Waka Kamichatani¹

¹Department of Health Chemistry, Showa Pharmaceutical University, Machida, Tokyo 194-8543, Japan.

International Journal of Molecular Sciences

|December 30, 2025

Summary

This study compared how fatty acids and 15d-PGJ2 activate peroxisome proliferator-activated receptors (PPARα/δ/γ). Palmitic acid and other key fatty acids activate PPARs at relevant concentrations, differing from synthetic agonists.

Keywords:

15-deoxy-Δ12,14-prostaglandin J2 coactivator recruitment endogenous ligand ligand-binding domain non-esterified fatty acids nuclear receptor peroxisome proliferator-activated receptor therapeutics time-resolved fluorescence resonance energy transfer transcriptional factor

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Area of Science:

Molecular Endocrinology
Lipid Metabolism
Nuclear Receptor Signaling

Background:

Peroxisome proliferator-activated receptors (PPARα/δ/γ) are nuclear receptors crucial for metabolic regulation.
Endogenous fatty acids (FAs) are known ligands, but comparative activation profiles are scarce.
Synthetic PPAR agonists exhibit varying coactivator recruitment, differing from natural ligands.

Purpose of the Study:

To comparatively analyze the activation of PPARα/δ/γ by 14 major free long-chain fatty acids (LCFAs) and 15-deoxy-Δ^12,14-prostaglandin J2 (15d-PGJ2).
To investigate ligand-concentration-dependent coactivator (PGC1α, CBP, SRC1, TRAP220) recruitment for PPAR subtypes.
To compare the coactivator preference of natural FA ligands versus synthetic PPAR agonists.

Main Methods:

Utilized a coactivator recruitment assay to assess PPARα/δ/γ activation.
Tested 15 potential ligands including 14 LCFAs (C12:0-C22:6) and 15d-PGJ2.
Examined the dose-dependent recruitment of four distinct coactivator peptides.

Main Results:

All 15 FAs activated PPARα/δ at high concentrations; palmitic, stearic, oleic, and linoleic acids showed significant activation at physiological concentrations.
Lauric, myristic, palmitic acids, and 15d-PGJ2 activated PPARγ at high concentrations; only palmitic acid showed slight activation at physiological concentrations.
FA ligands displayed different coactivator preferences compared to synthetic PPAR agonists (e.g., pemafibrate, seladelpar, pioglitazone).

Conclusions:

Specific LCFAs like palmitic acid are potent physiological activators of PPARα/δ and PPARγ.
Natural FA ligands exhibit distinct coactivator recruitment profiles compared to synthetic PPAR agonists.
Differences in coactivator recruitment may explain varying therapeutic effects and potential side effects of synthetic PPAR modulators.