Abstract
Patients suffering from traumatic brain injury (TBI) have decreased markers of energy metabolism, including N-acetylaspartate (NAA) and ATP. In the nervous system, NAA-derived acetate provides acetyl-CoA required for myelin lipid synthesis. Acetate can also be oxidized in mitochondria for the derivation of metabolic energy. In the current study, using the controlled cortical impact model of TBI in rats, we investigated the effects of the hydrophobic acetate precursor, glyceryltriacetate (GTA), as a method of delivering metabolizable acetate to the injured brain. We found that GTA administration significantly increased the levels of both NAA and ATP in the injured hemisphere 4 and 6 days after injury, and also resulted in significantly improved motor performance in rats 3 days after injury.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Acetates / pharmacology*
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Acetates / therapeutic use
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Acetic Acid / metabolism*
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Acetyl Coenzyme A / biosynthesis*
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Animals
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Aspartic Acid / analogs & derivatives
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Aspartic Acid / metabolism
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Brain / drug effects*
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Brain / metabolism
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Brain / physiopathology
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Brain Injuries / drug therapy*
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Brain Injuries / metabolism
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Brain Injuries / physiopathology
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Disease Models, Animal
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Energy Metabolism / drug effects
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Energy Metabolism / physiology
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Lipid Metabolism / drug effects
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Lipid Metabolism / physiology
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Male
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Membrane Lipids / biosynthesis
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Myelin Sheath / metabolism
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Neuroprotective Agents / pharmacology
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Neuroprotective Agents / therapeutic use
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Rats
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Rats, Sprague-Dawley
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Treatment Outcome
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Triacetin / pharmacology*
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Triacetin / therapeutic use
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Up-Regulation / drug effects
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Up-Regulation / physiology
Substances
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Acetates
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Membrane Lipids
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Neuroprotective Agents
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Aspartic Acid
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Acetyl Coenzyme A
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N-acetylaspartate
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Acetic Acid
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Triacetin