Modulation of oxidative stress and mitochondrial function by the ketogenic diet.
Study Goal
The researchers aimed to explore the potential mechanisms by which the ketogenic diet (KD) achieves neuroprotection and seizure control, focusing on mitochondrial functions and redox signaling.
Results Summary
The study suggests that the KD may influence mitochondrial functions and activate adaptive pathways like Nrf2, leading to increased production of antioxidants and detoxification enzymes, which could mediate its protective effects in epilepsy.
Population
Patients with intractable epilepsy.
Effective Dosage
Not specified
Duration
Not specified
Interactions
None mentioned
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
ketogenic diet (KD) | neutral | neuroprotection and/or seizure control | patients with intractable epilepsy | - | achieves | #1 |
ketogenic diet (KD) | neutral | diverse epilepsies | - | - | has broad efficacy in | #2 |
ketogenic diet (KD) | neutral | metabolism | - | - | has profound influence on | #3 |
ketogenic diet (KD) | neutral | mitochondrial functions | - | - | regulates | #4 |
ketogenic diet (KD) | neutral | redox signaling | - | - | regulates | #5 |
ketogenic diet (KD) | neutral | low levels of redox signaling molecules such as H(2)O(2) and electrophiles e.g. 4-hydroxynonenal (4-HNE) | - | - | involves the production of | #6 |
low levels of redox signaling molecules such as H(2)O(2) and electrophiles e.g. 4-hydroxynonenal (4-HNE) | increase | adaptive pathways such as the protective transcription factor, NF E2-related factor 2 (Nrf2) | - | - | activate | #7 |
activation of adaptive pathways such as the protective transcription factor, NF E2-related factor 2 (Nrf2) | increase | antioxidants (e.g. GSH) and detoxification enzymes | - | - | can ultimately result in increased production of | #8 |
increased production of antioxidants (e.g. GSH) and detoxification enzymes | neutral | the protective effects of the KD | - | - | may be critical in mediating | #9 |
The ketogenic diet (KD) is a high-fat, low carbohydrate diet that is used as a therapy for intractable epilepsy. However, the mechanism(s) by which the KD achieves neuroprotection and/or seizure control are not yet known. The broad efficacy of the KD in diverse epilepsies coupled with its profound influence on metabolism suggests that mitochondrial functions may be critical in its mechanism(s) of seizure control. Mitochondria subserve important cellular functions that include the production of cellular ATP, control of apoptosis, maintenance of calcium homeostasis and the production and elimination of reactive oxygen species (ROS). This review will focus on recent literature reporting the regulation of mitochondrial functions and redox signaling by the KD. The review highlights a potential mechanism of the KD involving the production of low levels of redox signaling molecules such as H(2)O(2) and electrophiles e.g. 4-hydroxynonenal (4-HNE), which in turn activate adaptive pathways such as the protective transcription factor, NF E2-related factor 2 (Nrf2). This can ultimately result in increased production of antioxidants (e.g. GSH) and detoxification enzymes which may be critical in mediating the protective effects of the KD.