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بدون خلاصۀ ویرایش |
بدون خلاصۀ ویرایش |
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A ketogenic diet has powerful anti-inflammatory activity and antioxidative stress effects in the brain. Jeong et al. found that a ketogenic diet reduced neuroinflammation via the activation of the peroxisome proliferator-activated receptor gamma (PPARγ) and protected against excitotoxicity-induced neuronal cell death. Fatty acids activate PPARs and are critical regulators of lipid metabolism. Greco et al. found that ketone bodies decreased oxidative stress and improved the mitochondrial respiratory complex activity in a traumatic brain injury animal model. A ketogenic diet likely normalizes mitochondrial function by stimulating mitochondrial biogenesis, decreasing oxidative stress and the levels of pro-apoptotic factors, preventing changes in mitochondrial permeability, and decreasing the mitochondrial ROS production in neocortical neurons. Mirza et al. showed that rats treated with propionic acid exhibited social impairment and repetitive behavior. The cerebellum, brainstem, and prefrontal cortex of these rats had high levels of oxidative stress and inflammation, with increased IL-6 and TNF-α levels and decreased IL-10 levels. They also found that decreased levels of oxidative stress and inflammation improved neurobehavioral disorders in rats. | A ketogenic diet has powerful anti-inflammatory activity and antioxidative stress effects in the brain. Jeong et al. found that a ketogenic diet reduced neuroinflammation via the activation of the peroxisome proliferator-activated receptor gamma (PPARγ) and protected against excitotoxicity-induced neuronal cell death. Fatty acids activate PPARs and are critical regulators of lipid metabolism. Greco et al. found that ketone bodies decreased oxidative stress and improved the mitochondrial respiratory complex activity in a traumatic brain injury animal model. A ketogenic diet likely normalizes mitochondrial function by stimulating mitochondrial biogenesis, decreasing oxidative stress and the levels of pro-apoptotic factors, preventing changes in mitochondrial permeability, and decreasing the mitochondrial ROS production in neocortical neurons. Mirza et al. showed that rats treated with propionic acid exhibited social impairment and repetitive behavior. The cerebellum, brainstem, and prefrontal cortex of these rats had high levels of oxidative stress and inflammation, with increased IL-6 and TNF-α levels and decreased IL-10 levels. They also found that decreased levels of oxidative stress and inflammation improved neurobehavioral disorders in rats. | ||
The Regulation of Neurotransmitters in the Brain | |||
GABA is the main inhibitory neurotransmitter in the brain, and it originates from glutamate decarboxylation. Glutamate is the primary excitatory neurotransmitter in the Central Nervous System. Patients with autism exhibited abnormal levels of proteins and messenger RNAs (mRNAs) associated with the glutamate system in the cerebellum. The medium-chain fatty acids that are present during the consumption of a ketogenic diet directly inhibit glutamate receptors and reduce seizures. Other studies found that beta-hydroxybutyrate, which is produced from a ketogenic diet, inhibited GABA degradation in astrocytes. One study showed that children with Autism spectrum disorder had reduced GABA levels in sensorimotor function, and this phenomenon was associated with poor tactile performance compared to healthy children. Autism spectrum disorder patients had significantly lower GABA concentrations in the auditory cortex. Patients with Autism spectrum disorder also had abnormal maturation of the neuronal circuitry on magnetoencephalography (MEG) and edited magnetic resonance spectroscopy (MRS). In summary, a ketogenic diet may ameliorate Autism spectrum disorder behaviors via the modulation of neurotransmitters, such as increasing GABA levels. | |||