Source:http://linkedlifedata.com/resource/pubmed/id/15341516
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2004-9-2
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pubmed:abstractText |
Creatine kinase (CK)-catalysed ATP-phosphocreatine (PCr) exchange is considered to play a key role in energy homeostasis of the brain. This study assessed the metabolic and anatomical consequences of partial or complete depletion of this system in transgenic mice without cytosolic B-CK (B-CK-/-), mitochondrial ubiquitous CK (UbCKmit-/-), or both isoenzymes (CK -/-), using non-invasive quantitative magnetic resonance (MR) imaging and spectroscopy. MR imaging revealed an increase in ventricle size in a subset of B-CK-/- mice, but not in animals with UbCKmit or compound CK mutations. Mice lacking single CK isoenzymes had normal levels of high-energy metabolites and tissue pH. In the brains of CK double knockouts pH and ATP and Pi levels were also normal, even though PCr had become completely undetectable. Moreover, a 20-30% decrease was observed in the level of total creatine and a similar increase in the level of neuronal N-acetyl-aspartate compounds. Although CKs themselves are not evenly distributed throughout the CNS, these alterations were uniform and concordant across different brain regions. Changes in myo-inositol and glutamate peaks did appear to be mutation type and brain area specific. Our results challenge current models for the biological significance of the PCr-CK energy system and suggest a multifaceted role for creatine in the brain.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Creatine,
http://linkedlifedata.com/resource/pubmed/chemical/Creatine Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/Creatine Kinase, BB Form,
http://linkedlifedata.com/resource/pubmed/chemical/Creatine Kinase, Mitochondrial Form,
http://linkedlifedata.com/resource/pubmed/chemical/Isoenzymes,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphorus Isotopes,
http://linkedlifedata.com/resource/pubmed/chemical/Tritium
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0022-3042
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
90
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1321-30
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:15341516-Animals,
pubmed-meshheading:15341516-Brain,
pubmed-meshheading:15341516-Brain Chemistry,
pubmed-meshheading:15341516-Creatine,
pubmed-meshheading:15341516-Creatine Kinase,
pubmed-meshheading:15341516-Creatine Kinase, BB Form,
pubmed-meshheading:15341516-Creatine Kinase, Mitochondrial Form,
pubmed-meshheading:15341516-Isoenzymes,
pubmed-meshheading:15341516-Magnetic Resonance Imaging,
pubmed-meshheading:15341516-Mice,
pubmed-meshheading:15341516-Mice, Inbred C57BL,
pubmed-meshheading:15341516-Mice, Knockout,
pubmed-meshheading:15341516-Nuclear Magnetic Resonance, Biomolecular,
pubmed-meshheading:15341516-Phosphorus Isotopes,
pubmed-meshheading:15341516-Tritium
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pubmed:year |
2004
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pubmed:articleTitle |
Cerebral creatine kinase deficiency influences metabolite levels and morphology in the mouse brain: a quantitative in vivo 1H and 31P magnetic resonance study.
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pubmed:affiliation |
Department of Radiology, Nijmegen Centre for Molecular Life Science, University Medical Centre Nijmegen, University of Nijmegen, Nijmegen, The Netherlands.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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