围产期α-亚麻酸缺乏与高脂肪饮食摄入对大鼠组织特异性脂肪酸谱的影响：母代和子代分析

IF 3.2

Prostaglandins, leukotrienes, and essential fatty acids Pub Date : 2026-04-01 Epub Date: 2026-01-19 DOI:10.1016/j.plefa.2026.102723

María Paz Beyer , Lorena Mercado-Lopez , Camila Farias , Robinson Carrasco-Gutiérrez , Alejandra Espinosa , Alexies Dagnino-Subiabre , Yasna Muñoz , Ignacio Alvear E , Luis A. Videla , Rodrigo Valenzuela

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引用次数: 0

摘要

饮食中omega-6 （n-6）与omega-3 （n-3）多不饱和脂肪酸（PUFAs）比例失衡和/或高脂肪饮食（HFD）可能会破坏必需PUFAs（如亚油酸（LA）和α-亚麻酸（ALA））向其长链衍生物（LC-PUFAs）的代谢转化，从而改变其在各组织中的积累。确定母体ALA和/或HFD低摄入量对大鼠母体组织（肝脏、脂肪组织和红细胞）和后代组织（肝脏、红细胞、脂肪组织、心脏、肾脏、肠道、肌肉、大脑、眼睛、肺和胃内容物）中FA组成的影响。方法采用前瞻性、随机、对照实验方法对Sprague-Dawley大鼠进行研究。动物被分配到四个饮食干预组中的一个：CD- 1%-ALA、CD-2%- ala、HFD- 1%-ALA和HFD-2%- ala。这些饮食在整个妊娠期、妊娠期和产后进行。安乐死后，收集组织样品，用气相色谱法分析FA组成。结果n-3 PUFAs的积累在分析的组织中有所不同，表明ALA的吸收或掺入具有组织特异性。大鼠肝脏的PUFA生物合成能力最高，而肝外组织的活性有限。此外，母亲的饮食与后代体内的多聚脂肪酸浓度并不一致。结论ALA的增加是组织特异性的，反映了组织类型的差异。母体n-3 PUFA储存成为将这些fa转移给后代的关键来源，特别是在饮食应激条件下，如低ALA摄入量或HFDs。

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Impact of perinatal α-linolenic acid deficiency combined with high-fat diet consumption on tissue-specific fatty acid profiles in rats: Maternal and offspring analysis

Background

An imbalance in the dietary ratio of omega-6 (n-6) to omega-3 (n-3) polyunsaturated fatty acids (PUFAs) and/or a high-fat diet (HFD) may disrupt the metabolic conversion of essential PUFAs, such as linoleic acid (LA) and α-linolenic acid (ALA), into their long-chain derivatives (LC-PUFAs), thereby altering their accumulation in various tissues. To determine the effects of low maternal intake of ALA and/or an HFD on FA composition in maternal tissues (liver, adipose tissue, and erythrocytes) and offspring tissues (liver, erythrocytes, adipose tissue, heart, kidney, intestine, muscle, brain, eye, lung, and stomach contents) in rats.

Methods

A prospective, randomized, controlled experimental study was conducted in Sprague-Dawley rats. Animals were assigned to one of four dietary intervention groups: CD-<1%-ALA, CD-2%-ALA, HFD-<1%-ALA, and HFD-2%-ALA. The diets were administered throughout the pregestational, gestational, and postnatal periods. Following euthanasia, tissue samples were collected and analyzed for FA composition using gas chromatography.

Results

The accumulation of n-3 PUFAs varied across the analyzed tissues, suggesting tissue-specific uptake or incorporation of ALA. The liver exhibited the highest capacity for PUFA biosynthesis in rats, whereas extrahepatic tissues showed limited activity. Moreover, maternal diet did not consistently correlate with PUFA concentrations in the offspring.

Conclusions

The increase in ALA is tissue-specific, reflecting differential incorporation among tissue types. Maternal n-3 PUFA stores become a critical source for the transfer of these FAs to the offspring, particularly under dietary stress conditions such as low ALA intake or HFDs.

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