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A more recent version of this article appeared on January 1, 2007

Papers In Press, published online ahead of print October 2, 2006
J. Lipid Res., doi:10.1194/jlr.M600050-JLR200
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Submitted on January 31, 2006
Revised on September 27, 2006
Accepted on October 1, 2006

Metabolism of phytol to phytanic acid in the mouse and the role of PPARalpha in its regulation

Jolein Gloerich, Daan M. van den Brink, Jos P. N. Ruiter, Naomi van Vlies, Frédéric M. Vaz, Ronald J. A. Wanders, and Sacha Ferdinandusse

Lab. Genetic Metabolic Diseases, Academic Medical Center, Amsterdam 1100 DE

Corresponding Author: s.ferdinandusse{at}amc.uva.nl

Phytol, a branched-chain fatty alcohol, is the naturally occurring precursor of phytanic and pristanic acid, branched-chain fatty acids which are both ligands for the nuclear hormone receptor peroxisome proliferator-activated receptor alpha (PPARalpha ). To investigate the metabolism of phytol and the role of PPARalpha in its regulation, wild-type and PPARalpha knockout (PPARalpha -/-) mice were fed a phytol-enriched diet or, for comparison, a diet enriched with Wy-14,643, a synthetic PPARalpha agonist. Following the phytol-enriched diet, phytol could only be detected in small intestine, the site of uptake, and liver. Upon longer duration of the diet, the level of the (E)-isomer of phytol increased significantly in the liver of PPARalpha -/- mice compared to wild-type mice. Activity measurements of the enzymes involved in phytol metabolism showed that treatment with a PPARalpha agonist resulted in a PPARalpha -dependent induction of at least two steps of the phytol degradation pathway in liver. Furthermore, the enzymes involved showed a higher activity towards the (E)-isomer than the (Z)-isomer of their respective substrates, indicating a stereospecificity towards the metabolism of (E)-phytol. In conclusion, the results described in this paper show that the conversion of phytol to phytanic acid is regulated via PPARalpha , and is specific for the breakdown of (E)-phytol.


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