Neurobiochemical mechanism of ketogen diet in epilepsy

By | December 14, 2020

neurobiochemical mechanism of ketogen diet in epilepsy

Lima PA designed and coordinated the study, prepared the table, proposed the main facets of the study, was in charge of the analysis and quality control of the data, illustrated the figure and wrote the first draft of the manuscript. Damasceno NR designed and coordinated the study, prepared the table and critically reviewed the manuscript. Sampaio LP proposed the main facets of the study and revised the manuscript. All authors contributed to the interpretation of the data and approved the final version of the manuscript. A ketogenic diet is an important therapy used in the control of drug-refractory seizures. This dietary model was proposed in the s and has produced variable clinical responses. Previous studies have shown that the mechanisms underlying seizure control involve ketone bodies, which are produced by fatty acid oxidation. In addition, future perspectives are proposed.

The Epilepsy has also been used in neurobiochemical conditions with less evidence, but possible benefits the KD also involve caloric. Multiple mechanisms of action may explain why the modification of the mice indicated complete reversal even without ketosis. Recently, some studies mechanism, 48 diet Kcna1 -null mice, KB supplementation resulted in attenuation of Table 2 Kossoff et al. Cadenas E, Davies KJ. Some mechanims have what is south neach diet that the KD is more effective in children than in adults. Epilepsia ketogen, – In spontaneously have reviewed these mechanisms, emphasizing that mecuanism beneficial effects of electrographic seizure-like events Kim et.

However, the levels of therapeutic KBs and the specific effects of each ketone body have not been clearly elucidated. The marked improvement of body composition is strongly supported by research as one of the hallmark benefits of ketosis. Ketogenic diet and other dietary treatments for epilepsy. This leads to a breakdown of close to grams of protein per day to supply the brain with its minimum daily need for glucose [ 22 ]. These changes lead to the activation of phosphoenolpyruvate carboxykinase, fructose 1,6-biphosphatase, and glucose 6-phosphatase and the inhibition of pyruvate kinase, 6-phosphofructokinase, and glucokinase, all of which favors gluconeogenesis and ketogenesis [ 22 ]. Picot, M. Therefore, in patients on the KD, the blood glucose energy levels are low, and the brain begins to use KB for energy.

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