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首页> 外文期刊>Journal of Neurochemistry: Offical Journal of the International Society for Neurochemistry >Dietary n-6 polyunsaturated fatty acid deprivation increases docosahexaenoic acid metabolism in rat brain.
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Dietary n-6 polyunsaturated fatty acid deprivation increases docosahexaenoic acid metabolism in rat brain.

机译：饮食中n-6多不饱和脂肪酸的缺乏会增加大鼠大脑中二十二碳六烯酸的代谢。

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摘要

Dietary n-6 polyunsaturated fatty acid (PUFA) deprivation in rodents reduces brain arachidonic acid (20:4n-6) concentration and 20:4n-6-preferring cytosolic phospholipase A(2) (cPLA(2) -IVA) and cyclooxygenase (COX)-2 expression, while increasing brain docosahexaenoic acid (DHA, 22:6n-3) concentration and DHA-selective calcium-independent phospholipase A(2) (iPLA(2) )-VIA expression. We hypothesized that these changes are accompanied by up-regulated brain DHA metabolic rates. Using a fatty acid model, brain DHA concentrations and kinetics were measured in unanesthetized male rats fed, for 15 weeks post-weaning, an n-6 PUFA 'adequate' (31.4 wt% linoleic acid) or 'deficient' (2.7 wt% linoleic acid) diet, each lacking 20:4n-6 and DHA. [1-(14) C]DHA was infused intravenously, arterial blood was sampled, and the brain was microwaved at 5 min and analyzed. Rats fed the n-6 PUFA deficient compared with adequate diet had significantly reduced n-6 PUFA concentrations in brain phospholipids but increased eicosapentaenoic acid (EPA, 20:5n-3), docosapentaenoic acid n-3 (DPAn-3, 22:5n-3), and DHA (by 9.4%) concentrations, particularly in ethanolamine glycerophospholipid (EtnGpl). Incorporation rates of unesterified DHA from plasma, which represent DHA metabolic loss from brain, were increased 45% in brain phospholipids, as was DHA turnover. Increased DHA metabolism following dietary n-6 PUFA deprivation may increase brain concentrations of antiinflammatory DHA metabolites, which with a reduced brain n-6 PUFA content, likely promotes neuroprotection and alters neurotransmission.
机译：啮齿动物中的膳食n-6多不饱和脂肪酸（PUFA）剥夺可降低脑花生四烯酸（20：4n-6）的浓度和20：4n-6优选的胞质磷脂酶A（2）（cPLA（2）-IVA）和环氧合酶（ COX）-2的表达，同时增加脑二十二碳六烯酸（DHA，22：6n-3）的浓度和DHA-选择性钙非依赖性磷脂酶A（2）（iPLA（2））-VIA表达。我们假设这些变化伴随着大脑DHA代谢率的上调。使用脂肪酸模型，在断奶后喂养15周的未麻醉雄性大鼠中测量n-6 PUFA“充足”（31.4 wt％亚油酸）或“不足”（2.7 wt％亚油酸）的脑DHA浓度和动力学。酸）饮食，每种都缺乏20：4n-6和DHA。静脉内注入[1-（14）C] DHA，取样动脉血，然后在5分钟内对大脑进行微波处理并进行分析。与充足饮食相比，n-6 PUFA缺乏的大鼠的脑磷脂中n-6 PUFA的浓度明显降低，但二十碳五烯酸（EPA，20：5n-3），二十碳五烯酸n-3（DPAn-3，22：5n）升高。 -3）和DHA（9.4％）的浓度，尤其是在乙醇胺甘油磷脂（EtnGpl）中。血浆中未酯化DHA的掺入率（代表大脑中DHA的代谢损失）与DHA周转率一样，在脑磷脂中增加了45％。饮食中n-6 PUFA被剥夺后DHA代谢增加可能会增加脑中抗炎DHA代谢物的浓度，而脑n-6 PUFA含量降低会促进神经保护作用并改变神经传递。

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