Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bldg. 9, Room 1S126, Bethesda, MD 20892, USA.
Prostaglandins Leukot Essent Fatty Acids. 2011 Dec;85(6):361-8. doi: 10.1016/j.plefa.2011.08.002. Epub 2011 Aug 30.
Knowing threshold changes in brain lipids and lipid enzymes during dietary n-3 polyunsaturated fatty acid deprivation may elucidate dietary regulation of brain lipid metabolism. To determine thresholds, rats were fed for 15 weeks DHA-free diets having graded reductions of α-linolenic acid (α-LNA). Compared with control diet (4.6% α-LNA), plasma DHA fell significantly at 1.7% dietary α-LNA while brain DHA remained unchanged down to 0.8% α-LNA, when plasma and brain docosapentaenoic acid (DPAn-6) were increased and DHA-selective iPLA(2) and COX-1 activities were downregulated. Brain AA was unchanged by deprivation, but AA selective-cPLA(2), sPLA(2) and COX-2 activities were increased at or below 0.8% dietary α-LNA, possibly in response to elevated brain DPAn-6. In summary, homeostatic mechanisms appear to maintain a control brain DHA concentration down to 0.8% dietary DHA despite reduced plasma DHA, when DPAn-6 replaces DHA. At extreme deprivation, decreased brain iPLA(2) and COX-1 activities may reduce brain DHA loss.
了解膳食 n-3 多不饱和脂肪酸缺乏时脑脂质和脂质酶的阈值变化可能阐明膳食对脑脂质代谢的调节作用。为了确定阈值,大鼠连续 15 周喂食缺乏 DHA 的饮食,其中 α-亚麻酸(α-LNA)逐渐减少。与对照饮食(4.6%α-LNA)相比,当饮食中 α-LNA 降低至 0.8%时,血浆 DHA 显著下降,而脑 DHA 保持不变,此时血浆和脑二十二碳五烯酸(DPAn-6)增加,DHA 选择性 iPLA(2) 和 COX-1 活性下调。脑 AA 不受缺乏的影响,但 AA 选择性-cPLA(2)、sPLA(2) 和 COX-2 活性在 0.8%饮食 α-LNA 或以下时增加,可能是由于脑 DPAn-6 升高所致。总之,尽管血浆 DHA 减少,但当 DPAn-6 替代 DHA 时,内稳态机制似乎可以维持脑 DHA 浓度在 0.8%饮食 DHA 以下的控制水平。在极端缺乏的情况下,脑 iPLA(2) 和 COX-1 活性的降低可能会减少脑 DHA 的丢失。