Metabolic acetate therapy for the treatment of traumatic brain injury
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 deriva...
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| Veröffentlicht in: | Journal of neurotrauma 2010-01, Vol.27 (1), p.293-298 |
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| container_title | Journal of neurotrauma |
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| creator | Arun, Peethambaran Ariyannur, Prasanth S Moffett, John R Xing, Guoqiang Hamilton, Kristen Grunberg, Neil E Ives, John A Namboodiri, Aryan M A |
| description | 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. |
| doi_str_mv | 10.1089/neu.2009.0994 |
| format | Article |
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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.</description><identifier>ISSN: 0897-7151</identifier><identifier>EISSN: 1557-9042</identifier><identifier>DOI: 10.1089/neu.2009.0994</identifier><identifier>PMID: 19803785</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Acetates ; Acetates - pharmacology ; Acetates - therapeutic use ; Acetic Acid - metabolism ; Acetyl Coenzyme A - biosynthesis ; Animals ; Aspartic Acid - analogs & derivatives ; Aspartic Acid - metabolism ; Brain ; Brain - drug effects ; Brain - metabolism ; Brain - physiopathology ; Brain damage ; Brain Injuries - drug therapy ; Brain Injuries - metabolism ; Brain Injuries - physiopathology ; Disease Models, Animal ; Energy Metabolism - drug effects ; Energy Metabolism - physiology ; Health aspects ; Injuries ; Lipid Metabolism - drug effects ; Lipid Metabolism - physiology ; Male ; Membrane Lipids - biosynthesis ; Metabolism ; Mitochondrial DNA ; Myelin Sheath - metabolism ; Neurology ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; Pharmacology ; Physiological aspects ; Rats ; Rats, Sprague-Dawley ; Rodents ; Short Communications ; Treatment Outcome ; Triacetin - pharmacology ; Triacetin - therapeutic use ; Up-Regulation - drug effects ; Up-Regulation - physiology</subject><ispartof>Journal of neurotrauma, 2010-01, Vol.27 (1), p.293-298</ispartof><rights>COPYRIGHT 2010 Mary Ann Liebert, Inc.</rights><rights>(©) Copyright 2010, Mary Ann Liebert, Inc.</rights><rights>Copyright 2010, Mary Ann Liebert, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c546t-9862103588191b6bf4888ce73447d2f1b7ae70598ae8b2588196fb820a65083a3</citedby><cites>FETCH-LOGICAL-c546t-9862103588191b6bf4888ce73447d2f1b7ae70598ae8b2588196fb820a65083a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19803785$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Arun, Peethambaran</creatorcontrib><creatorcontrib>Ariyannur, Prasanth S</creatorcontrib><creatorcontrib>Moffett, John R</creatorcontrib><creatorcontrib>Xing, Guoqiang</creatorcontrib><creatorcontrib>Hamilton, Kristen</creatorcontrib><creatorcontrib>Grunberg, Neil E</creatorcontrib><creatorcontrib>Ives, John A</creatorcontrib><creatorcontrib>Namboodiri, Aryan M A</creatorcontrib><title>Metabolic acetate therapy for the treatment of traumatic brain injury</title><title>Journal of neurotrauma</title><addtitle>J Neurotrauma</addtitle><description>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.</description><subject>Acetates</subject><subject>Acetates - pharmacology</subject><subject>Acetates - therapeutic use</subject><subject>Acetic Acid - metabolism</subject><subject>Acetyl Coenzyme A - biosynthesis</subject><subject>Animals</subject><subject>Aspartic Acid - analogs & derivatives</subject><subject>Aspartic Acid - metabolism</subject><subject>Brain</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Brain - physiopathology</subject><subject>Brain damage</subject><subject>Brain Injuries - drug therapy</subject><subject>Brain Injuries - metabolism</subject><subject>Brain Injuries - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Energy Metabolism - drug effects</subject><subject>Energy Metabolism - physiology</subject><subject>Health aspects</subject><subject>Injuries</subject><subject>Lipid Metabolism - drug effects</subject><subject>Lipid Metabolism - physiology</subject><subject>Male</subject><subject>Membrane Lipids - biosynthesis</subject><subject>Metabolism</subject><subject>Mitochondrial DNA</subject><subject>Myelin Sheath - metabolism</subject><subject>Neurology</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Pharmacology</subject><subject>Physiological aspects</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Short Communications</subject><subject>Treatment Outcome</subject><subject>Triacetin - pharmacology</subject><subject>Triacetin - therapeutic use</subject><subject>Up-Regulation - drug effects</subject><subject>Up-Regulation - physiology</subject><issn>0897-7151</issn><issn>1557-9042</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkc1LAzEQxYMoWqtHr7LoeWsmm2ySiyDiFyhe9ByyaVJTupuazQr9701t8QMkh8xkfvN44SF0AngCWMiLzg4TgrGcYCnpDhoBY7yUmJJdNMpzXnJgcIAO-36OMVQ14fvoAKTAFRdshG6ebNJNWHhTaJPLZIv0ZqNergoX4rouUrQ6tbZLRXC50UOrU8abqH1X-G4-xNUR2nN60dvj7T1Gr7c3L9f35ePz3cP11WNpGK1TKUVNAFdMCJDQ1I2jQghjeUUpnxIHDdeWYyaFtqIhX1jtGkGwrhkWla7G6HKjuxya1k5NNhX1Qi2jb3VcqaC9-jvp_JuahQ9FBKEEZBY42wrE8D7YPql5GGKXPSuQFCgXQDJ0voFmemGV71zIWqb1vVFXBETNgDCeqck_VD5T23oTOut8fv-zUG4WTAx9H6379g1YrbNUOUu1zlKts8z86e_P_tDb8KpPrDGYuQ</recordid><startdate>201001</startdate><enddate>201001</enddate><creator>Arun, Peethambaran</creator><creator>Ariyannur, Prasanth S</creator><creator>Moffett, John R</creator><creator>Xing, Guoqiang</creator><creator>Hamilton, Kristen</creator><creator>Grunberg, Neil E</creator><creator>Ives, John A</creator><creator>Namboodiri, Aryan M A</creator><general>Mary Ann Liebert, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>201001</creationdate><title>Metabolic acetate therapy for the treatment of traumatic brain injury</title><author>Arun, Peethambaran ; Ariyannur, Prasanth S ; Moffett, John R ; Xing, Guoqiang ; Hamilton, Kristen ; Grunberg, Neil E ; Ives, John A ; Namboodiri, Aryan M A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c546t-9862103588191b6bf4888ce73447d2f1b7ae70598ae8b2588196fb820a65083a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Acetates</topic><topic>Acetates - 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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.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>19803785</pmid><doi>10.1089/neu.2009.0994</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acetates Acetates - pharmacology Acetates - therapeutic use Acetic Acid - metabolism Acetyl Coenzyme A - biosynthesis Animals Aspartic Acid - analogs & derivatives Aspartic Acid - metabolism Brain Brain - drug effects Brain - metabolism Brain - physiopathology Brain damage Brain Injuries - drug therapy Brain Injuries - metabolism Brain Injuries - physiopathology Disease Models, Animal Energy Metabolism - drug effects Energy Metabolism - physiology Health aspects Injuries Lipid Metabolism - drug effects Lipid Metabolism - physiology Male Membrane Lipids - biosynthesis Metabolism Mitochondrial DNA Myelin Sheath - metabolism Neurology Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Pharmacology Physiological aspects Rats Rats, Sprague-Dawley Rodents Short Communications Treatment Outcome Triacetin - pharmacology Triacetin - therapeutic use Up-Regulation - drug effects Up-Regulation - physiology |
| title | Metabolic acetate therapy for the treatment of traumatic brain injury |
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