Muller-Schwarze A B, Tandon P, Liu Z, Yang Y, Holmes G L, Stafstrom C E
Department of Neurology, Children's Hospital and Medical Center, Boston, MA, USA.
Neuroreport. 1999 May 14;10(7):1517-22. doi: 10.1097/00001756-199905140-00023.
The high fat, low carbohydrate, low protein ketogenic diet (KD) has been used to control refractory epilepsy in children since 1920, although its mechanism of action is unknown. Previous animal studies have shown that the KD can increase acute seizure threshold, but the effect of the KD on the process of epileptogenesis has not been studied. We tested the effect of an experimental KD on epileptogenesis in adult rats using the kainic acid (KA) model. P54 rats underwent KA-induced status epilepticus, followed by assignment to a control diet or a KD consisting of (by weight), 14% protein, 70% fat and no carbohydrate. KD-fed animals tolerated the diet and maintained ketosis. KD-fed rats had significantly fewer and briefer spontaneous recurrent seizures and less supragranular mossy fiber sprouting, although the degree of hippocampal pyramidal cell damage was similar in both groups. These results provide the first evidence that the KD retards epileptogenesis in an experimental model.
自1920年以来，高脂肪、低碳水化合物、低蛋白的生酮饮食（KD）就被用于控制儿童难治性癫痫，尽管其作用机制尚不清楚。以往的动物研究表明，生酮饮食可提高急性癫痫发作阈值，但尚未研究生酮饮食对癫痫发生过程的影响。我们使用海藻酸（KA）模型测试了实验性生酮饮食对成年大鼠癫痫发生的影响。54日龄大鼠经历KA诱导的癫痫持续状态，随后被分配到对照饮食组或由14%蛋白质、70%脂肪且不含碳水化合物组成的生酮饮食组。喂食生酮饮食动物能够耐受该饮食并维持酮症状态。喂食生酮饮食的大鼠自发性复发性癫痫发作明显减少且持续时间更短，颗粒上层苔藓纤维出芽也更少，尽管两组海马锥体细胞损伤程度相似。这些结果首次证明生酮饮食在实验模型中可延缓癫痫发生。
