Access restrictions were established for this page. If you see this message, you have no access to this page.
بدون خلاصۀ ویرایش |
بدون خلاصۀ ویرایش |
||
| خط ۱۱: | خط ۱۱: | ||
The Neuroprotective Role of a ketogenic diet in the Central Nervous System | The Neuroprotective Role of a ketogenic diet in the Central Nervous System | ||
A ketogenic diet contains abundant fat and induces the generation of acetyl-CoA in the mitochondria of the liver via fatty acid oxidation. Therefore, abundant acetyl-CoA is shunted to the formation of ketone bodies (acetoacetate, β-hydroxybutyrate, and acetone) in the liver. These ketone bodies enter into the circulation and are used to produce energy. One of the main ketones is acetone, which increases the seizure threshold and potentiates the anticonvulsant activity of some antiepileptic drugs. Therefore, fatty acids and ketone bodies exert neuroprotective effects in the brain. For example, ketone bodies improve the energy metabolism by enhancing ATP production and normalizing mitochondrial function via the stimulation of mitochondrial biogenesis and the reduction of oxidative stress, which reduces neuronal death. Ketone bodies regulate neurotransmitters, increase γ-aminobutyric acid (GABA) levels, and inhibit the activation of the mammalian target of rapamycin (mTOR) signaling pathway. However, the exact neuroprotective mechanisms of a ketogenic diet are not fully understood. | A ketogenic diet contains abundant fat and induces the generation of acetyl-CoA in the mitochondria of the liver via fatty acid oxidation. Therefore, abundant acetyl-CoA is shunted to the formation of ketone bodies (acetoacetate, β-hydroxybutyrate, and acetone) in the liver. These ketone bodies enter into the circulation and are used to produce energy. One of the main ketones is acetone, which increases the seizure threshold and potentiates the anticonvulsant activity of some antiepileptic drugs. Therefore, fatty acids and ketone bodies exert neuroprotective effects in the brain. For example, ketone bodies improve the energy metabolism by enhancing ATP production and normalizing mitochondrial function via the stimulation of mitochondrial biogenesis and the reduction of oxidative stress, which reduces neuronal death. Ketone bodies regulate neurotransmitters, increase γ-aminobutyric acid (GABA) levels, and inhibit the activation of the mammalian target of rapamycin (mTOR) signaling pathway. However, the exact neuroprotective mechanisms of a ketogenic diet are not fully understood. | ||
The Improvement of Energy Metabolism in the Central Nervous System | |||
Autism spectrum disorder individuals have impaired mitochondrial energy production due to the presence of abnormal mitochondrial markers in their plasma, such as elevated levels of lactic acid and pyruvate. Weissman et al. showed that Autism spectrum disorder patients had mitochondrial electron transport chain dysfunction, including complex I and complex III deficiencies. A ketogenic diet provides fuel sources in the human body, and the ketone bodies, including β-hydroxybutyrate, cross the blood-brain barrier and replace glucose as fuel for the brain. This molecule crosses the blood-brain barrier via proton symporters and a sodium-dependent monocarboxylate transporter, which is located in the blood-brain barrier, neurons, and astrocytes. Ketone bodies enhance adenosine triphosphate (ATP) production via the Krebs cycle to generate energy and balance metabolism. A ketogenic diet reduced seizures by enhancing brain metabolism via the regulation of transcripts encoding energy metabolism enzymes or mitochondrial proteins in rats with seizures. | |||