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首页> 外文期刊>Journal of Lipid Research >Phospholipid supplementation reverses behavioral and biochemical alterations induced by n-3 polyunsaturated fatty acid deficiency in mice.
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Phospholipid supplementation reverses behavioral and biochemical alterations induced by n-3 polyunsaturated fatty acid deficiency in mice.

机译：补充磷脂可逆转小鼠n-3多不饱和脂肪酸缺乏引起的行为和生化改变。

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This study investigated the effects of a diet deficient in alpha-linolenic acid followed or not by supplementation with phospholipids rich in n-3 polyunsaturated fatty acids (PUFA) on behavior and phospholipid fatty acid composition in selected brain regions. Three weeks before mating, two groups of mice were fed a semisynthetic diet containing both linoleic and alpha-linolenic acid or a diet deficient in alpha-linolenic acid. Pups were fed the same diet as their dams. At the age of 7 weeks, a part of the deficient group was supplemented with n-3 PUFA from either egg yolk or pig brain phospholipids for 2 months. In the open field, rearing activity was significantly reduced in the deficient group. In the elevated plus maze (anxiety protocol), the time spent on open arms was significantly smaller in deficient mice than in controls. Using the learning protocol with the same task, the alpha-linolenic acid deficiency induced a learning deficit. Rearing activity and learning deficits were completely restored by supplementation with egg yolk or cerebral phospholipids, though the level of anxiety remained significantly higher than that of controls. There were no differences among the 4 diet groups for either the Morris water maze or passive avoidance. In control mice, the level of 22:6 n-3 was significantly higher in the frontal cortex compared to all other regions analysed. The frontal cortex and the striatum were the most markedly affected by the deficiency. Supplementation with phospholipids restored normal fatty acid composition in brain regions except for frontal cortex. Egg yolk or cerebral phospholipids are an effective source of n-3 PUFA for reversing behavioral changes and altered fatty acid composition induced by a diet deficient in n-3 PUFA.
机译：这项研究调查了缺乏α-亚麻酸的饮食，然后补充或不补充富含n-3多不饱和脂肪酸（PUFA）的磷脂对某些大脑区域行为和磷脂脂肪酸组成的影响。交配前三周，给两组小鼠喂食含有亚油酸和α-亚麻酸的半合成饮食或缺乏α-亚麻酸的饮食。幼犬的饮食与大坝相同。在7周大的时候，一部分缺陷人群补充了来自蛋黄或猪脑磷脂的n-3 PUFA，为期2个月。在旷野中，缺乏者的饲养活动明显减少。在高架迷宫中（焦虑方案），缺陷小鼠的张开双臂所花费的时间明显少于对照组。使用具有相同任务的学习协议，α-亚麻酸缺乏症会导致学习不足。补充蛋黄或脑磷脂可完全恢复饲养活动和学习障碍，尽管焦虑水平仍显着高于对照组。对于莫里斯水迷宫或被动回避，这四个饮食组之间没有差异。在对照小鼠中，与所有其他分析区域相比，额叶皮层中22：6 n-3的水平明显更高。额叶和纹状体受缺损影响最明显。补充磷脂可恢复大脑额叶皮层以外的正常脂肪酸组成。蛋黄或脑磷脂是n-3 PUFA的有效来源，可逆转由n-3 PUFA缺乏饮食引起的行为改变和脂肪酸组成改变。

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