Metabolic Acetate Therapy for the Treatment of Traumatic Brain Injury

被引：57

作者：

Arun, Peethambaran ^{[1
,2
]}

Ariyannur, Prasanth S. ^{[1
,2
]}

Moffett, John R. ^{[1
,2
]}

Xing, Guoqiang ^{[3
]}

Hamilton, Kristen ^{[4
]}

Grunberg, Neil E. ^{[4
]}

Ives, John A. ^{[5
]}

Namboodiri, Aryan M. A. ^{[1
,2
]}

机构：

[1] Uniformed Serv Univ Hlth Sci, Dept Anat Physiol & Genet, Neurosci Program, Bethesda, MD 20814 USA

[2] Uniformed Serv Univ Hlth Sci, Mol & Cell Biol Program, Bethesda, MD 20814 USA

[3] Uniformed Serv Univ Hlth Sci, Dept Psychiat, Bethesda, MD 20814 USA

[4] Uniformed Serv Univ Hlth Sci, Dept Med & Clin Psychol, Bethesda, MD 20814 USA

[5] Samueli Inst, Alexandria, VA USA

来源：

JOURNAL OF NEUROTRAUMA | 2010年 / 27卷 / 01期

关键词：

ATP; glyceryltriacetate; myelin synthesis; N-acetylaspartate; CONTROLLED CORTICAL IMPACT; N-ACETYLASPARTATE; MITOCHONDRIAL DYSFUNCTION; KETOGENIC DIET; RATS; SYNTHETASE; OXIDATION; SEVERITY; PROTEINS; JUVENILE;

D O I：

10.1089/neu.2009.0994

中图分类号：

R4 [临床医学];

学科分类号：

100218 [急诊医学];

摘要：

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.

引用

页码：293 / 298

页数：6

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