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The aim of the subsequent study was to identify a PPARalpha ligand under EFA deficiency. Lysophospholipids (lysoPL) are the most likely candidates for the ligands because decreased HUFA under EFA deficiency may shift the equilibrium of phospholipid deacylation/reacylation cycle toward accumulation of lysoPL. To test the hypothesis, first we used computer simulation to estimate affinity between lysoPL and PPARalpha. The model predicted lysoPL binding with high affinity. Next, binding affinity of lysoPL to PPARalpha was measured in vitro using a fluorescent ligand displacement assay. The dissociation constants (Kd) of lysoPL were low nanomolar suggesting that they are potent ligands for PPARalpha. Finally, when CV-1 cells were treated with lysoPL, a reporter plasmid with PPARalpha response elements was induced. In conclusion, our study suggests that PPARalpha, together with SREBP-1c, senses HUFA status and confers pathway specific induction of HUFA synthesis by EFA deficient diets. LysoPL may act as signaling molecule and activate PPARalpha in response to essential fatty acid deficiency.
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