The ketogenic diet and epilepsy
The ketogenic diet and epilepsy
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DOI：
10.1097/mco.0b013e3282f44c06
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发表时间：
2008-03-01
影响因子：
3.1
通讯作者：
Rho, Jong M.
中科院分区：
文献类型：
--
作者：
Kim, Do Young;Rho, Jong M.
综述目的生酮饮食长期以来一直用于治疗难治性癫痫。然而，其临床作用的机制仍然是一个谜。迄今为止的证据表明，生酮饮食诱导的从糖酵解到中间代谢的根本转变对于临床疗效是必要和充分的。越来越多的研究表明，葡萄糖限制，酮体和多不饱和脂肪酸可能都发挥了机械作用，可能通过增强线粒体呼吸和ATP的产生，并减少活性氧的产生。酮体可以减弱中枢神经元中ATP敏感性钾通道的自发放电，并且在大鼠点燃模型中已经显示出对糖酵解的药理学抑制可以延缓癫痫发生。越来越多的证据表明，生酮饮食改变了神经元的基本生物化学，不仅抑制了神经元的过度兴奋，而且还产生保护作用。因此，生酮饮食可能最终可用于治疗各种神经系统疾病。
Purpose of reviewThe ketogenic diet has long been used to treat medically refractory epilepsy. The mechanisms underlying its clinical effects, however, have remained a mystery. The evidence to date suggests that a fundamental shift from glycolysis to intermediary metabolism induced by the ketogenic diet is necessary and sufficient for clinical efficacy. This notion is supported by a growing number of studies indicating that glucose restriction, ketone bodies and polyunsaturated fatty acids may all play mechanistic roles, possibly by enhancing mitochondrial respiration and ATP production, and decreasing reactive oxygen species production.Recent findingsRecent reports indicate that ketone bodies can reduce oxidative stress and that fatty acid-induced mitochondrial uncoupling may also yield similar protective effects. Ketone bodies may attenuate spontaneous firing of ATP-sensitive potassium channels in central neurons, and pharmacological inhibition of glycolysis has been shown to retard epileptogenesis in a rat kindling model.SummaryWhile the mechanisms underlying the broad clinical efficacy of the ketogenic diet remain unclear, there is growing evidence that the ketogenic diet alters the fundamental biochemistry of neurons in a manner that not only inhibits neuronal hyperexcitability but also induces a protective effect. Thus, the ketogenic diet may ultimately be useful in the treatment of a variety of neurological disorders.