Specifically, fatty acid oxidation may not keep up with required rapid ATP generation during periods of extended continuous and rapid neuronal firing, making it less suitable than glucose oxidation for brain metabolism [119]
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This viewpoint has been supported by observations of reduced mitochondrial ROS production and improved human bronchial EpiC viability with treatment using a CPT1A inhibitor, etomoxir, after CS exposure (Jiang et al., 2017)