Cullingford Tim E
Faculty of Pharmaceutical Sciences, Department of Clinical and Molecular Pharmacokinetics/Pharmacodynamics, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Prostaglandins Leukot Essent Fatty Acids. 2004 Mar;70(3):253-64. doi: 10.1016/j.plefa.2003.09.008.
This review outlines the molecular sensors that reprogram cellular metabolism in response to the ketogenic diet (KD). Special emphasis is placed on the fasting-, fatty acid- and drug-activated transcription factor, peroxisome proliferator-activated receptor alpha (PPARalpha). The KD causes a switch to ketogenesis that is coordinated with an array of changes in cellular lipid, amino acid, carbohydrate and inflammatory pathways. The role of both liver and brain PPARalpha in mediating such changes will be examined, with special reference to the anti-epileptic effects not only of the KD but a range of synthetic anti-epileptic drugs such as valproate. Finally, the implications of the KD and activated brain PPARalpha will be discussed in the context of their potential involvement in a range of disorders of neuro-degeneration and neuro-inflammation.
本综述概述了响应生酮饮食（KD）而重新编程细胞代谢的分子传感器。特别强调了禁食、脂肪酸和药物激活的转录因子——过氧化物酶体增殖物激活受体α（PPARα）。生酮饮食会导致代谢转变为酮生成，这与细胞脂质、氨基酸、碳水化合物和炎症途径的一系列变化相协调。将研究肝脏和大脑中的PPARα在介导此类变化中的作用，特别提及生酮饮食以及一系列合成抗癫痫药物（如丙戊酸盐）的抗癫痫作用。最后，将在生酮饮食和激活的大脑PPARα可能参与一系列神经退行性疾病和神经炎症性疾病的背景下，讨论它们的影响。
