Decreased liver peroxisomal β-oxidation accompanied by changes in brain fatty acid composition in aged rats

Peroxisomal β-oxidation is primarily responsible for the degradation of very long chain fatty acids (VLCFAs), dicarboxylic acids, unsaturated fatty acids and branched fatty acids. The genes encoding β-oxidation enzymes are transcriptionally regulated by peroxisome proliferator-activated receptor alpha (PPARα). Age-related decreases in acyl-CoA oxidase 1 (ACOX1) activity, a key enzyme involved in peroxisomal β-oxidation, have been found in aged rodents. To determine whether decreased peroxisomal β-oxidation with aging affects brain fatty acid composition, 22-month-old (old) and 3-month-old (young) male Sprague–Dawley rats were used. We confirmed the decreased expression of liver ACOX1 and PPARα in old rats. In addition, a gas chromatography assay showed significant changes in the percentage of fatty acids in the cerebral cortices between old and young rats. In the cerebral cortices of old rats, the increased fatty acids included VLCFAs (C20:0, C22:0, C24:0) and monounsaturated fatty acids (C16:1, C18:1, C20:1, C22:1, C24:1), whereas the decreased fatty acids included C18:0, C20:4 and C22:6. These results indicated that decreased liver peroxisomal β-oxidation was accompanied by changes in brain fatty acid composition with aging and suggested that peroxisomal β-oxidation dysfunction may play a potential role in the progression of brain aging.