Rudy Luna, Carmen Rubio, Daniel Rojas, Artemio Rosiles, Moisés Rubio-Osornio
Departamento de Neurofisiología, Instituto Nacional de Neurología y Neurocirugía, M.V.S. México City, Mexico.
Laboratorio Experimental de Enfermedades Neurodegenerativas, Instituto Nacional de Neurología y Neurocirugía, M.V.S. México City, Mexico.
Epilepsy Res. 2020 Dec;168:106499. doi: 10.1016/j.eplepsyres.2020.106499. Epub 2020 Nov 1.
Many treatments have been proposed to control epileptic seizures, such as the ketogenic diet and caloric restriction. However, seizure control has not yet been improved completely in all patients. Probably, due to the lack of understanding regarding this neurological disorder pathogenesis or pathophysiology, including its molecular approach. Currently, there is not much information about the molecular processes and genes involved, and their relation to the possible beneficial effects of diet therapy on epilepsy. The ketogenic diet and caloric restriction are implicated in potential anti-seizure mechanisms related to the gut microbiome, metabolic pathways, hormones and neurotransmitters, mitochondria improvement, a role in inflammation, and oxidative stress, among others. In this review, we pretend to describe the molecular mechanism and the possible genes involved in the different ketogenic diet and caloric restriction mechanisms of action described to decrease neural excitability and, therefore, epileptic seizures, especially when conventional treatment is not enough to achieve control of epilepsy.
已经提出了许多治疗方法来控制癫痫发作，如生酮饮食和热量限制。然而，并非所有患者的癫痫发作控制都得到了完全改善。这可能是由于对这种神经疾病的发病机制或病理生理学缺乏了解，包括其分子层面的情况。目前，关于所涉及的分子过程和基因及其与饮食疗法对癫痫可能的有益作用之间的关系，信息还不多。生酮饮食和热量限制与潜在的抗癫痫发作机制有关，这些机制涉及肠道微生物群、代谢途径、激素和神经递质、线粒体改善、在炎症中的作用以及氧化应激等。在这篇综述中，我们旨在描述在不同的生酮饮食和热量限制作用机制中涉及的分子机制和可能的基因，这些机制被描述为可降低神经兴奋性，从而减少癫痫发作，尤其是在常规治疗不足以控制癫痫的情况下。
