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Amino Acids. 2017 Jan;49(1):1-20. doi: 10.1007/s00726-016-2336-7. Epub 2016 Sep 28.

Control of seizures by ketogenic diet-induced modulation of metabolic pathways.

Author information

1
Department of Nuclear Engineering, Texas A&M University, College Station, TX, 77843, USA. rc1025@tamu.edu.
2
Systems Radiobiology Laboratory, Texas A&M Institute for Preclinical Studies, Texas A&M University, 800 Raymond Stotzer Parkway, College Station, TX, 77843, USA. rc1025@tamu.edu.
3
Department of Biology, Texas A&M University, Room 412A, Building BSBW, College Station, TX, 77843-3258, USA. rc1025@tamu.edu.
4
Department of Animal Sciences, Texas A&M University, College Station, TX, 77843, USA.
5
Department of Medical Physiology, Texas A&M University, College Station, TX, 77843, USA.
6
Department of Nuclear Engineering, Texas A&M University, College Station, TX, 77843, USA.
7
Systems Radiobiology Laboratory, Texas A&M Institute for Preclinical Studies, Texas A&M University, 800 Raymond Stotzer Parkway, College Station, TX, 77843, USA.
8
Departments of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX, 77843, USA.
9
Department of Biology, Texas A&M University, Room 412A, Building BSBW, College Station, TX, 77843-3258, USA. raramayo@tamu.edu.

Abstract

Epilepsy is too complex to be considered as a disease; it is more of a syndrome, characterized by seizures, which can be caused by a diverse array of afflictions. As such, drug interventions that target a single biological pathway will only help the specific individuals where that drug's mechanism of action is relevant to their disorder. Most likely, this will not alleviate all forms of epilepsy nor the potential biological pathways causing the seizures, such as glucose/amino acid transport, mitochondrial dysfunction, or neuronal myelination. Considering our current inability to test every individual effectively for the true causes of their epilepsy and the alarming number of misdiagnoses observed, we propose the use of the ketogenic diet (KD) as an effective and efficient preliminary/long-term treatment. The KD mimics fasting by altering substrate metabolism from carbohydrates to fatty acids and ketone bodies (KBs). Here, we underscore the need to understand the underlying cellular mechanisms governing the KD's modulation of various forms of epilepsy and how a diverse array of metabolites including soluble fibers, specific fatty acids, and functional amino acids (e.g., leucine, D-serine, glycine, arginine metabolites, and N-acetyl-cysteine) may potentially enhance the KD's ability to treat and reverse, not mask, these neurological disorders that lead to epilepsy.

KEYWORDS:

Epilepsy; Hypomyelination; Ketogenic diet; Ketone bodies; Malate-aspartate shuttle; Medium chain fatty acids; Mitochondrial disorders; Monocarboxylic acid transporters; Short chain fatty acids

PMID:
27683025
DOI:
10.1007/s00726-016-2336-7
[Indexed for MEDLINE]

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