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Unlike even\u2010chain fatty acids metabolized to acetyl\u2010CoA only, triheptanoin can indeed provide both acetyl\u2010CoA and propionyl\u2010CoA, two key carbon sources for the Krebs cycle. Triheptanoin was initially used in patients with long\u2010chain fatty acid oxidation disorders. The first demonstration of the possible benefit of triheptanoin for brain energy deficit came from a patient with pyruvate carboxylase deficiency, a severe metabolic disease that affects anaplerosis in the brain. In an open\u2010label study, triheptanoin was then shown to decrease nonepileptic paroxysmal manifestations by 90% in patients with glucose transporter 1 deficiency syndrome, a disease that affects glucose transport into the brain. <jats:sup>31<\/jats:sup>P magnetic resonance spectroscopy studies also indicated that triheptanoin was able to correct bioenergetics in the brain of patients with Huntington disease, a neurodegenerative disease associated with brain energy deficit. 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