{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T13:49:51Z","timestamp":1784728191285,"version":"3.55.0"},"reference-count":43,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2005,7,25]],"date-time":"2005-07-25T00:00:00Z","timestamp":1122249600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2005,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Pyruvate given in large doses may be neuroprotective in stroke, but it is not known to what degree the brain metabolizes pyruvate. Intravenous injection of [3\u2010<jats:sup>13<\/jats:sup>C]pyruvate led to dose\u2010dependent labelling of cerebral metabolites so that at 5\u2003min after injection of 18\u2003mmoles [3\u2010<jats:sup>13<\/jats:sup>C]pyruvate\/kg (2\u2003g sodium pyruvate\/kg), approximately 20% of brain glutamate and GABA were labelled, as could be detected by <jats:sup>13<\/jats:sup>C nuclear magnetic resonance spectrometry <jats:italic>ex vivo<\/jats:italic>. Pyruvate, 9\u2003mmoles\/kg, was equivalent to glucose, 9\u2003mmoles\/kg, as a substrate for cerebral tricarboxylic acid (TCA) cycle activity. Inhibition of the glial TCA cycle with fluoroacetate did not affect formation of [4\u2010<jats:sup>13<\/jats:sup>C]glutamate or [2\u2010<jats:sup>13<\/jats:sup>C]GABA from [3\u2010<jats:sup>13<\/jats:sup>C]pyruvate, but reduced formation of [4\u2010<jats:sup>13<\/jats:sup>C]glutamine by 50%, indicating predominantly neuronal metabolism of exogenous pyruvate. Extensive formation of [3\u2010<jats:sup>13<\/jats:sup>C]lactate from [2\u2010<jats:sup>13<\/jats:sup>C]pyruvate demonstrated reversible carboxylation of pyruvate to malate and equilibration with fumarate, presumably in neurones, but anaplerotic formation of TCA cycle intermediates from exogenous pyruvate could not be detected. Too rapid injection of large amounts of pyruvate led to seizure activity, respiratory arrest and death. We conclude that exogenous pyruvate is an excellent energy substrate for neurones <jats:italic>in vivo<\/jats:italic>, but that care must be taken to avoid the seizure\u2010inducing effect of pyruvate given in large doses.<\/jats:p>","DOI":"10.1111\/j.1471-4159.2005.03365.x","type":"journal-article","created":{"date-parts":[[2005,9,9]],"date-time":"2005-09-09T10:06:49Z","timestamp":1126260409000},"page":"284-293","source":"Crossref","is-referenced-by-count":66,"title":["Brain metabolism of exogenous pyruvate"],"prefix":"10.1111","volume":"95","author":[{"given":"Susana Villa","family":"Gonzalez","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nga H. 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