Other indirect ways to stimulate the antiepileptic effects of KD may lay in the alterations of the metabolism of neurotransmitters such as glutamate and gamma-amino butyric acid (GABA), and the activation of energy-sensing signaling pathways such as the PPAR, mammalian target of rapamycin (mTOR), and adenosine monophosphate-(AMP)-activated kinase (AMPK) pathways (71, 72)
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When cells are over-nutrient and hyperglycemic, the excessive NADH produced by the polyol pathway will promote the production of superoxide through the overload complex I of ETC, resulting in cell dysfunction and impaired insulin secretion
