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胎儿大脑中二十二碳六烯酸积聚的机制。

Mechanisms of docosahexaenoic acid accretion in the fetal brain.

作者信息

Green P, Yavin E

机构信息

Department of Internal Medicine B, The Rabin Medical Center (Beilinson Campus) Petah Tikva and the Sackler School of Medicine, Tel-Aviv University, Israel.

出版信息

J Neurosci Res. 1998 Apr 15;52(2):129-36. doi: 10.1002/(SICI)1097-4547(19980415)52:2<129::AID-JNR1>3.0.CO;2-C.

DOI:10.1002/(SICI)1097-4547(19980415)52:2<129::AID-JNR1>3.0.CO;2-C
PMID:9579403
Abstract

Docosahexaenoic acid (DHA, 22:6 n-3) is the major polyunsaturated fatty acid (PUFA) in the adult mammalian brain. DHA is an essential fatty acid (FA) since it, or its short chain precursor, alpha-linolenic acid (LnA, 18:3 n-3), have to be obtained in the diet. Moreover, dietary n-3 FA deficiency is associated with biochemical changes in the brain and with disturbances in vision and other neurological parameters. Under normal nutritional conditions, fetal brain DHA accumulation is substantial, with a "DHA accretion spurt" being demonstrated in the last period of gestation. This accumulation is supported by the maternal supply of DHA or LnA, but selectivity of DHA accumulation is probably a placental function whose mechanism is lately being clarified. The fetal gastrointestinal (G-I) tract may be instrumental in supplying DHA to the fetal brain under certain conditions, such as following intra-amniotic administration of ethyl-docosahexaenoate (Et-DHA). In this pathway, DHA is supplied independently of the maternal metabolism, and the fetal liver is apparently involved. The fetal G-I tract may be advantageous for DHA supply in cases of maternal-placental insufficiency resulting in intrauterine growth retardation. The fetal brain itself is capable of metabolizing LnA to DHA, without the participation of the fetal liver, thus contributing to the accumulation of its own DHA during one of the most crucial periods of its development.

摘要

二十二碳六烯酸(DHA,22:6 n-3)是成年哺乳动物大脑中的主要多不饱和脂肪酸(PUFA)。DHA是一种必需脂肪酸(FA),因为它或其短链前体α-亚麻酸(LnA,18:3 n-3)必须从饮食中获取。此外,膳食n-3脂肪酸缺乏与大脑中的生化变化以及视力和其他神经学参数的紊乱有关。在正常营养条件下,胎儿大脑中的DHA积累量很大,在妊娠后期会出现“DHA积累激增”。这种积累得到母体提供的DHA或LnA的支持,但DHA积累的选择性可能是一种胎盘功能,其机制最近正在得到阐明。在某些情况下,如羊膜腔内注射二十二碳六烯酸乙酯(Et-DHA)后,胎儿胃肠道(G-I)可能有助于向胎儿大脑供应DHA。在这条途径中,DHA的供应独立于母体代谢,胎儿肝脏显然也参与其中。在导致宫内生长迟缓的母体-胎盘功能不全的情况下,胎儿胃肠道可能有利于DHA的供应。胎儿大脑本身能够在不依赖胎儿肝脏参与的情况下将LnA代谢为DHA,从而在其发育的最关键时期之一促进自身DHA的积累。

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