Boosting the injured brain with supplemental energy fuels

Excerpt

Clinical investigation, using cerebral metabolic assessment with positron emission tomography, magnetic resonance spectroscopy, and regional cerebral microdialysis, has repeatedly disclosed major alterations of cerebral energy metabolism in the aftermath of traumatic brain injury (TBI). Impairment of cerebral energy metabolism is characterized by elevated cerebral glucose demand, increased glycolysis, and diversion of the main substrate, glucose, to be used in injury-related reparative pathways, such as the pentose phosphate pathway. Ultimately, these secondary processes lead to a reduction of the cerebral metabolic rate of glucose and a decreased availability of cerebral extracellular glucose. To compensate for glucose shortage, cerebral lactate metabolism and uptake are increased in patients with TBI [1]. Use of alternative cerebral energy substrates—including lactate (LAC), but also ketone bodies (KB) such as β-hydroxybutyrate (BHB) and acetoacetate (AcAc)—may therefore be a key adaptive mechanism following TBI. …