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脂肪酸氧化与癫痫。

Fatty acid oxidation and epilepsy.

机构信息

Inserm, U676, Paris, France.

出版信息

Epilepsy Res. 2012 Jul;100(3):224-8. doi: 10.1016/j.eplepsyres.2011.05.022. Epub 2011 Aug 19.

DOI:10.1016/j.eplepsyres.2011.05.022
PMID:21856124
Abstract

The ketogenic diet (KD) is a high-fat and low carbohydrate diet with an established efficacy to treat refractory epilepsy. Lipids, particularly fatty acids, are nutrients which provide the most important part of the caloric intake under the KD. It has been suggested that the 'high-fat' component of the KD plays a role in its anticonvulsant properties. It has been shown experimentally that polyunsaturated fatty acids alone (PUFA) exhibit anticonvulsant properties. But clinical trials in epilepsy using PUFA have failed to show any effect. This discrepancy can be explained by recent experimental data. Several experimental studies have suggested that PUFA may support the efficacy of the KD. PUFA may exhibit anticonvulsant properties via various mechanisms such as a modification of the composition of the CNS cell membranes, stimulation of nuclear receptor such as PPAR and by attenuating inflammation. Most of these hypotheses have evolved from experimental studies. However, it remains necessary to prove the role of PUFA in the KD, and therefore, further studies on this subject are needed. A better understanding of the underlying mechanisms may lead to the design new dietary treatment such as more liberal rules for KD or KD formula with a higher efficacy.

摘要

生酮饮食(KD)是一种高脂肪、低碳水化合物的饮食,已被证实可有效治疗难治性癫痫。脂肪,尤其是脂肪酸,是 KD 下提供大部分热量摄入的重要营养素。有人认为 KD 的“高脂肪”成分在其抗惊厥特性中起作用。实验表明,单独的多不饱和脂肪酸(PUFA)具有抗惊厥特性。但在癫痫中使用 PUFA 的临床试验未能显示出任何效果。这种差异可以用最近的实验数据来解释。几项实验研究表明,PUFA 可能支持 KD 的疗效。PUFA 可以通过改变 CNS 细胞膜的组成、刺激核受体(如 PPAR)和减轻炎症等多种机制发挥抗惊厥作用。这些假设大多来自于实验研究。然而,仍有必要证明 PUFA 在 KD 中的作用,因此需要对此主题进行进一步的研究。对潜在机制的更好理解可能会导致设计新的饮食治疗方法,例如对 KD 或 KD 配方有更宽松的规则,以提高其疗效。

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