Bough K J, Eagles D A
Department of Biology, Georgetown University, Washington, DC 20057-1229, USA.
Epilepsia. 1999 Feb;40(2):138-43. doi: 10.1111/j.1528-1157.1999.tb02066.x.
The purpose of this study was to test the hypothesis that a ketogenic diet would increase the resistance of rats to pentylenetetrazole (PTZ)-induced seizures and to understand the relation of ketonemia to seizure resistance.
A freely consumed, high-fat (ketogenic) diet was administered to male Sprague-Dawley rats for 5-10 weeks, while control animals were fed either rodent chow or a high-carbohydrate diet. Ketonemia was measured as plasma levels of beta-hydroxybutyric acid (beta-OHB). Seizures were induced by tail-vein infusion of pentylenetetrazole.
The ketogenic diet produced a highly significant (p<0.01) increase in beta-OHB levels within 5 days. Induction of seizures by PTZ 35 days after animals were placed on their respective diets showed that ketogenic animals had a significantly (p<0.01) increased threshold for seizure induction compared with those fed an isocaloric diet of either high-carbohydrate or normal rodent chow. Ketogenic animals did not exhibit increased seizure severity relative to controls, despite receiving consistently higher doses of PTZ.
The ketogenic diet resulted in an increased seizure threshold, confirming the hypothesis, and seizure threshold was found to be a direct function of the level of ketonemia.
本研究旨在验证生酮饮食可增强大鼠对戊四氮（PTZ）诱导癫痫发作的抵抗力这一假设，并了解酮血症与癫痫抵抗力之间的关系。
对雄性斯普拉格 - 道利大鼠给予可自由摄取的高脂肪（生酮）饮食，持续5 - 10周，而对照动物则喂食啮齿动物饲料或高碳水化合物饮食。酮血症通过测量血浆中β - 羟基丁酸（β - OHB）水平来评估。通过尾静脉注射戊四氮诱导癫痫发作。
生酮饮食在5天内使β - OHB水平显著升高（p<0.01）。在动物开始各自饮食35天后，用PTZ诱导癫痫发作，结果显示，与喂食等热量高碳水化合物饮食或正常啮齿动物饲料的动物相比，生酮饮食的动物癫痫发作诱导阈值显著升高（p<0.01）。尽管生酮饮食的动物持续接受更高剂量的PTZ，但与对照组相比，其癫痫发作严重程度并未增加。
生酮饮食导致癫痫发作阈值升高，证实了假设，且发现癫痫发作阈值是酮血症水平的直接函数。
