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首页> 外文期刊>Lipids >Chronic dietary n-3 polyunsaturated fatty acids deficiency affects the fatty acid composition of plasmenylethanolamine and phosphatidylethanolamine differently in rat frontal cortex, striatum, and cerebellum.
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Chronic dietary n-3 polyunsaturated fatty acids deficiency affects the fatty acid composition of plasmenylethanolamine and phosphatidylethanolamine differently in rat frontal cortex, striatum, and cerebellum.

机译:慢性饮食中的n-3多不饱和脂肪酸缺乏症对大鼠额叶皮层,纹状体和小脑的血浆烯基乙醇胺和磷脂酰乙醇胺的脂肪酸组成有不同的影响。

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摘要

As chronic consumption of a diet devoid of n-3 fatty acid induced modification of neurotransmission pathways in the frontal cortex of rats, plasmalogen alteration could occur in this area. Because of the propensity to facilitate membrane fusion, plasmenylethanolamine (PmE), a major plasmalogen of brain, may be involved in synaptic transmission. Female rats were fed diet containing peanut oil [(n-3)-deficient diet] through two generations. Two weeks before mating, half of the female rats of the second generation received a diet containing peanut oil and rapeseed oil (control group). The distribution and acyl composition of major phospholipids, phosphatidylethanolamine and PmE, were measured in the frontal cortex, striatum, and cerebellum of the male progeny of the two groups at 60 d of age. The n-3 polyunsaturated fatty acid (PUFA) deficiency had no effect on the distribution of phospholipids in all brain regions but affected their acyl composition differently. The level of 22:6n-3 was significantly lower and compensated for by higher levels of n-6 fatty acids in all regions and phospholipids studied. However, docosahexaenoic acid, being more concentrated in the PmE of frontal cortex, is also more decreased in the n-3-deficient rats compared to the striatum. By contrast, striatum PmE has retained more 22:6n-3 than PmE of the other regions. In addition, the increase of n-6 PUFA was significantly lower in frontal cortex PmE compared to the striatum and cerebellum PmE. In association with altered neurotransmission observed in frontal cortex of n-3-deficient rats, our results suggest that frontal cortex PmE might be more affected in chronically alpha-linolenic-deficient rats. However, by retaining 22:6n-3, striatum PmE could be most resilient.
机译:由于长期食用不含n-3脂肪酸的饮食会引起大鼠额叶皮质神经传递途径的改变,因此缩醛磷脂可能会在该区域发生改变。由于倾向于促进膜融合,因此,脑中主要的缩醛磷脂等离子乙醇胺(PmE)可能参与突触传递。雌性大鼠经过两代饲喂含有花生油的饮食[(n-3)缺乏饮食]。交配前两周,第二代雌性大鼠的一半接受了含有花生油和菜籽油的饮食(对照组)。在60岁时,测量了两组雄性子代的额叶皮层,纹状体和小脑中主要磷脂,磷脂酰乙醇胺和PmE的分布和酰基组成。 n-3多不饱和脂肪酸(PUFA)的缺乏对所有脑区中磷脂的分布没有影响,但对它们的酰基组成有不同的影响。在所有研究区域和所研究的磷脂中,22:6n-3的水平显着降低,并被较高水平的n-6脂肪酸补偿。然而,与纹状体相比,在n-3-缺陷大鼠中二十二碳六烯酸更集中在额叶皮层的PmE中,其含量也降低了更多。相比之下,纹状体PmE保留的22:6n-3比其他区域的PmE多。另外,与纹状体和小脑PmE相比,额叶皮层PmE中n-6 PUFA的增加明显更低。与在n-3缺陷大鼠的额皮质中观察到的神经传递改变相关,我们的结果表明,在慢性α-亚麻酸缺乏大鼠中额叶PmE可能受到更大的影响。但是,通过保留22:6n-3,纹状体PmE可能最具弹性。

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