School of Nursing, Xinxiang Medical University, Xinxiang, China.
Neurol Sci. 2014 Feb;35(2):289-93. doi: 10.1007/s10072-013-1509-3. Epub 2013 Jul 27.
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.
过氧化物酶体β-氧化主要负责降解超长链脂肪酸（VLCFAs）、二羧酸、不饱和脂肪酸和支链脂肪酸。β-氧化酶的基因受过氧化物酶体增殖物激活受体α（PPARα）转录调控。在老年啮齿动物中，已发现与年龄相关的酰基辅酶 A 氧化酶 1（ACOX1）活性下降，ACOX1 是过氧化物酶体β-氧化中的关键酶。为了确定衰老过程中过氧化物体β-氧化的减少是否会影响大脑脂肪酸组成，使用了 22 个月大（老年）和 3 个月大（年轻）的雄性 Sprague-Dawley 大鼠。我们证实了老年大鼠肝脏 ACOX1 和 PPARα 的表达减少。此外，气相色谱分析显示，老年和年轻大鼠大脑皮质中的脂肪酸百分比有显著变化。在老年大鼠的大脑皮质中，增加的脂肪酸包括超长链脂肪酸（C20:0、C22:0、C24:0）和单不饱和脂肪酸（C16:1、C18:1、C20:1、C22:1、C24:1），而减少的脂肪酸包括 C18:0、C20:4 和 C22:6。这些结果表明，肝脏过氧化物体β-氧化减少伴随着衰老时大脑脂肪酸组成的变化，表明过氧化物体β-氧化功能障碍可能在大脑衰老的进展中发挥潜在作用。
