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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5 Pt 1
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pubmed:dateCreated |
1997-7-8
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pubmed:abstractText |
Mitochondrial and cytosolic creatine kinase (CK) isozymes are active in cells with high and variable ATP metabolic rates. beta-Guanidinopropionic acid (GPA), a competitive inhibitor of creatine transport, was used to study the hypothesis that the creatine-CK-phosphocreatine (PCr) system is important in regulating brain ATP metabolism. The CK-catalyzed reaction rate and reactant concentrations were measured in vivo with 31P nuclear magnetic resonance spectroscopy during energy deficit (hypoxia) or high-energy turnover (seizures) states in urethane-anesthetized mice fed GPA, creatine, or standard chow (controls). Brain phosphagen (i.e., cellular energy reserves) or PCr plus phosphorylated GPA (GPAP) concentrations were equal. The phosphagen-to-NTP ratio was lower than in controls. In vivo CK reaction rate decreased fourfold, whereas ex vivo CK activity that was biochemically measured was doubled. During seizures, CK-catalyzed fluxes increased only in GPA-fed mice. Phosphagen increased in GPA-fed mice, whereas PCr decreased in controls. Survival was higher and brain phosphagen and ATP losses were less for hypoxic GPA-fed mice than for controls. In contrast to mice fed GPA, hypoxic survival and CK reactant concentrations during hypoxia and seizures were the same in creatine-fed mice and controls. Thus GPA, GPAP, or adaptive changes in ATP metabolism stabilize brain ATP and enhance survival during hypoxia in mice.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Creatine,
http://linkedlifedata.com/resource/pubmed/chemical/Creatine Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/Guanidines,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphocreatine,
http://linkedlifedata.com/resource/pubmed/chemical/Propionic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/guanidinopropionic acid
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
272
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
C1567-77
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9176148-Adenosine Triphosphate,
pubmed-meshheading:9176148-Animals,
pubmed-meshheading:9176148-Anoxia,
pubmed-meshheading:9176148-Brain,
pubmed-meshheading:9176148-Creatine,
pubmed-meshheading:9176148-Creatine Kinase,
pubmed-meshheading:9176148-Diet,
pubmed-meshheading:9176148-Female,
pubmed-meshheading:9176148-Guanidines,
pubmed-meshheading:9176148-Magnetic Resonance Spectroscopy,
pubmed-meshheading:9176148-Mice,
pubmed-meshheading:9176148-Mice, Inbred Strains,
pubmed-meshheading:9176148-Phosphocreatine,
pubmed-meshheading:9176148-Phosphorylation,
pubmed-meshheading:9176148-Propionic Acids,
pubmed-meshheading:9176148-Seizures
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pubmed:year |
1997
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pubmed:articleTitle |
In vivo brain phosphocreatine and ATP regulation in mice fed a creatine analog.
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pubmed:affiliation |
Department of Neurology, Children's Hospital, Boston, Massachusetts, USA. holtzman@al.tch.harvard.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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