AI Article Synopsis
- During fasting and intense exercise, brain cells switch their energy source from glucose to the ketone 3-hydroxybutyrate (3OHB).
- Studies indicate that 3OHB can protect neurons from damage caused by excitotoxicity and oxidative stress, but how it does this is not completely understood.
- 3OHB boosts mitochondrial respiration, which helps increase BDNF expression, a crucial factor for synaptic plasticity and neuronal resilience, suggesting it plays a role in how neurons adapt to fasting, exercise, and ketogenic diets.
Article Abstract
During fasting and vigorous exercise, a shift of brain cell energy substrate utilization from glucose to the ketone 3-hydroxybutyrate (3OHB) occurs. Studies have shown that 3OHB can protect neurons against excitotoxicity and oxidative stress, but the underlying mechanisms remain unclear. Neurons maintained in the presence of 3OHB exhibited increased oxygen consumption and ATP production, and an elevated NAD /NADH ratio. We found that 3OHB metabolism increases mitochondrial respiration which drives changes in expression of brain-derived neurotrophic factor (BDNF) in cultured cerebral cortical neurons. The mechanism by which 3OHB induces Bdnf gene expression involves generation of reactive oxygen species, activation of the transcription factor NF-κB, and activity of the histone acetyltransferase p300/EP300. Because BDNF plays important roles in synaptic plasticity and neuronal stress resistance, our findings suggest cellular signaling mechanisms by which 3OHB may mediate adaptive responses of neurons to fasting, exercise, and ketogenic diets.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5123937 | PMC |
| http://dx.doi.org/10.1111/jnc.13868 | DOI Listing |
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