ArticleMolecular biology reports2025
Neurochemical and genetic effects of the ketogenic diet: alterations in brain GABA, glutamate, and related gene.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Computational Modeling of Neurotransmitter Cycling Predicts Human Brain Glutamate and GABA Dynamics in Response to Acute Administration of Exogenous Ketones.Neurochemical research · 2026Article
- Potential Role of Mitochondria-Associated Endoplasmic Reticulum Membranes (MAMs) Abnormalities in Epileptogenesis: Multimodal Mechanisms and Therapeutic Targets.Molecular neurobiology · 2026Review
- Crosstalk Between Gut Microbiota, Epigenome, and Neurotransmitters in Health and Disease.Cells · 2026Review
- Ketogenic Diet and Neurological Health: A Narrative Review with Natural Language Processing-Assisted Thematic Mapping Using BERTopic.Neuropsychiatric disease and treatment · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA ketogenic diet (KD) is an effective nonpharmacological alternative therapy for managing drug-resistant epilepsy (DRE). We aimed to explore the potential effects of a KD on brain glutamate (Glu) and gamma-aminobutyric acid (GABA) neurotransmitters and their associated genes [glutamic acid decarboxylase (GAD) 65, GAD67, and GABA transaminase (GABA-T)] in rats as a possible antiseizure mechanism. METHODS AND
resultsEighteen male rats were divided into two weight-matched groups, namely, the normal diet (ND) group and the KD group. The ND group received a standard rat chow diet (10% protein, 80% carbohydrates, 10% fat; Kcal%). The KD group received a high-fat diet mimicking a clinical 4:1 fat to carbohydrate and protein ratio (8% protein, 2% carbohydrates, and 90% fat; Kcal%). The groups received diets for 30 days. The serum levels of beta-hydroxybutyric acid (BHB) in the KD group were significantly (p < 0.001) greater than those in the ND group. The brain concentrations of Glu and GABA in the KD group were lower (p = 0.001) and greater (p = 0.041), respectively. Compared with the ND group, the KD group presented increased GAD67 and decreased GABA-T levels (p = 0.036 and p = 0.035, respectively).
conclusionsThe elevated BHB observed with KD might be associated with changes in GABA and Glu levels in the brain, possibly reflecting alterations in GABA-T and GAD67 gene expression. These findings may provide preliminary insight into a mechanism that could contribute to the antiseizure effects of a KD.
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Registered trials
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