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Such benefits could have been achieved through different mechanisms promoted by KD, including an appetite reduction related to higher levels of glucagon-like peptide 1, cholecystokinin, and ghrelin (so-called “satiety” hormones), or perhaps caused by the suppression of the appetite promoted by ketones themselves [9,10]. Therefore, the KD-induced elevation of blood ketone bodies and fatty acids could potentially modulate neuronal membrane excitability through the activation of two-pore domain potassium channels . It has been supposed that the glycolytic adenosine triphosphate (ATP) production enhanced by the KD, and the reduced brain glucose utilization, induce ATP-sensitive potassium channels, increasing the epileptic threshold and then reducing seizures, as has been found in mouse models [19,20]. However, the impact of KD on the microbiota is still poorly understood, and it could represent a crucial feature in the effectiveness of this treatment. 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