2011年生酮饮食:它是如何工作的。

Epilepsy research and treatment Pub Date : 2011-01-01 Epub Date: 2011-06-05 DOI:10.1155/2011/963637
Keren Politi, Lilach Shemer-Meiri, Avinoam Shuper, S Aharoni
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引用次数: 20

摘要

虽然生酮饮食(KD)已被广泛接受为一种合法和成功的治疗癫痫和其他神经系统疾病的方法,但其作用机制仍然是一个谜。KD的使用引起了主要的代谢变化。其中最重要的似乎是慢性酮症,但也有其他的情况,例如,高水平的多不饱和脂肪酸(PUFAs)。这些"主要"影响导致"次要"影响,部分是适应性影响,例如线粒体密度和基因表达的变化。临床上,饮食的影响被认为是抗惊厥和神经保护,尽管神经保护也可以导致预防癫痫发作。讨论了这些机制的潜在临床意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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The ketogenic diet 2011: how it works.

Although the ketogenic diet (KD) has been widely accepted as a legitimate and successful therapy for epilepsy and other neurological disorders, its mechanism of action remains an enigma. The use of the KD causes major metabolic changes. The most significant of them seems to be the situation of chronic ketosis, but there are others as well, for instance, high level of polyunsaturated fatty acids (PUFAs). These "primary" influences lead to "secondary", in part adaptive, effects, for instance changes in mitochondrial density and gene expression. Clinically, the influences of the diet are considered as anticonvulsive and neuroprotective, although neuroprotection can also lead to prevention of seizures. Potential clinical implications of these mechanisms are discussed.

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