Phytanic acid (3, 7, 11, 15-tetramethylhexadecanoic acid, PA) is an aliphatic alcohol-related fatty acid whose four hydrogen atoms in the C16 backbone are replaced by methyl groups. In nature, PA is generated via oxidation of phytol, the side chain of chlorophyll, and some microorganisms inhabiting the rumen can release phytol from chlorophyll (Hellgren, 2010). There are two mechanisms of conversion of phytol to PA: the phytenic acid-producing pathway where phytol is sequentially oxidized to phytenal and phytenic acid and then reduced to PA, and the dihydrophytol-producing pathway where phytol is first reduced to dihydrophytol and then oxidized to phytanal and PA (Hellgren, 2010; van den Brink & Wanders, 2006; Vetter & Schröder, 2010). Conversion of phytol to PA also proceeds in the rumen (Patton & Benson, 1966), as the rumen is well-equipped to produce PA from chlorophyll, and the resultant PA is absorbed and translocated to the adipose tissue and milk of ruminants. Consequently, the concentrations of PA in dairy products and ruminant meat are significantly higher than those of other foods (Brown et al., 1993). Because humans are not capable of producing PA from chlorophyll, PA in humans is mainly derived from exogenous PA sources, especially the above dairy products and ruminant meat. Unlike normal fatty acids which are degraded by β-oxidation, catabolism of PA starts with α-oxidation to produce pristanic acid (PrA) which is then degraded by β-oxidation. Patients with Refsum disease have a mutation in the key enzyme of α-oxidation and show an abnormal accumulation of PA in plasma, leading to a neurocutaneous syndrome (Ferdinandusse et al., 2000). Therefore, elevated

The aims of this research communication were to investigate the in vivo tissue accumulation of phytanic acid (PA) and any changes in the tissue fatty acid profiles in mice. Previous in vitro studies have demonstrated that PA is a milk component with the potential to cause both beneficial effects on lipid and glucose metabolism and detrimental effects on neuronal cells. However, there is limited information about its in vivo actions. In this study, mice were fed diets containing either 0.00 or 0.05% 3RS, 7R, 11R-PA, which is the isomer found in milk and the human body. After 4 weeks, adipose tissue, liver and brain were harvested and their fatty acid profiles were determined by gas chromatographic analysis. The results showed that PA and its metabolite pristanic acid accumulated in the adipose tissue of PA-fed mice, and that dietary PA decreased the hepatic compositions of several saturated fatty acids such as palmitic acid while increasing the compositions of polyunsaturated fatty acids including linoleic acid and docosahexaenoic acid. However, dietary PA neither accumulated nor had a high impact on the fatty acid profile in the brain. These results suggested that dietary PA could exert its biological activities in adipose tissue and liver, although the brain is relatively less affected by dietary PA. These data provide a basis for understanding the in vivo physiological actions of PA.