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生酮饮食机制中的酮体、糖酵解和ATP敏感性钾通道

Ketone bodies, glycolysis, and KATP channels in the mechanism of the ketogenic diet.

作者信息

Yellen Gary

机构信息

Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA. gary

出版信息

Epilepsia. 2008 Nov;49 Suppl 8(Suppl 8):80-2. doi: 10.1111/j.1528-1167.2008.01843.x.

Abstract

The ketogenic diet (KD) has shown remarkable efficacy in the treatment of drug-resistant childhood epilepsy. Our understanding of how the KD produces its anticonvulsant and antiepileptogenic effects remains incomplete, which is perhaps not surprising for a biological manipulation as sweeping as dietary change. Several hypotheses focus on ketone bodies, fuel molecules that circulate at millimolar concentrations in the blood of patients on a KD, as causative agents. Here I consider some recent evidence for one such hypothesis, involving a possible role for altered glycolysis and consequent activation of a class of potassium channels called K(ATP)channels.

摘要

生酮饮食(KD)已在治疗儿童耐药性癫痫方面显示出显著疗效。我们对KD如何产生抗惊厥和抗癫痫作用的理解仍不完整,对于像饮食改变这样全面的生物操纵来说,这或许并不奇怪。有几种假说将焦点放在酮体上,酮体是KD患者血液中以毫摩尔浓度循环的燃料分子,认为它们是致病因素。在此,我探讨了支持其中一种假说的一些最新证据,该假说涉及糖酵解改变以及随之激活一类称为K(ATP)通道的钾通道的可能作用。

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