Yellen Gary
Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA. gary
Epilepsia. 2008 Nov;49 Suppl 8(Suppl 8):80-2. doi: 10.1111/j.1528-1167.2008.01843.x.
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.
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。