{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T18:00:08Z","timestamp":1787508008517,"version":"build-2736575974"},"reference-count":36,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2011,1,25]],"date-time":"2011-01-25T00:00:00Z","timestamp":1295913600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Inher Metab Disea"],"published-print":{"date-parts":[[2011,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Concentrations of glutarate (GA) and its derivatives such as 3\u2010hydroxyglutarate (3OHGA), D\u2010 (D\u20102OHGA) and L\u20102\u2010hydroxyglutarate (L\u20102OHGA) are increased in plasma, cerebrospinal fluid (CSF) and urine of patients suffering from different forms of organic acidurias. It has been proposed that these derivatives cause neuronal damage in these patients, leading to dystonic and dyskinetic movement disorders. We have recently shown that these compounds are eliminated by the kidneys via the human organic anion transporters, OAT1 and OAT4, and the sodium\u2010dependent dicarboxylate transporter 3, NaDC3. In neurons, where most of the damage occurs, a sodium\u2010dependent citrate transporter, NaCT, has been identified. Therefore, we investigated the impact of GA derivatives on hNaCT by two\u2010electrode voltage clamp and tracer uptake studies. None of these compounds induced substrate\u2010associated currents in hNaCT\u2010expressing\n                    <jats:italic>Xenopus laevis<\/jats:italic>\n                    oocytes nor did GA derivatives inhibit the uptake of citrate, the prototypical substrate of hNaCT. In contrast, D\u2010 and L\u20102OHGA, but not 3OHGA, showed affinities to NaDC3, indicating that D\u2010 and L\u20102OHGA impair the uptake of dicarboxylates into astrocytes thereby possibly interfering with their feeding of tricarboxylic acid cycle intermediates to neurons.\n                  <\/jats:p>","DOI":"10.1007\/s10545-010-9268-2","type":"journal-article","created":{"date-parts":[[2011,1,24]],"date-time":"2011-01-24T03:54:43Z","timestamp":1295841283000},"page":"477-482","source":"Crossref","is-referenced-by-count":16,"title":["The sodium\u2010dependent di\u2010 and tricarboxylate transporter, NaCT, is not responsible for the uptake of D\u2010, L\u20102\u2010hydroxyglutarate and 3\u2010hydroxyglutarate into neurons"],"prefix":"10.1002","volume":"34","author":[{"given":"Katja","family":"Brauburger","sequence":"first","affiliation":[{"name":"Zentrum Physiologie und Pathophysiologie, Abt. Vegetative Physiologie und Pathophysiologie Universit\u00e4tsmedizin G\u00f6ttingen Humboldtallee 23 G\u00f6ttingen 37073 Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerhard","family":"Burckhardt","sequence":"additional","affiliation":[{"name":"Zentrum Physiologie und Pathophysiologie, Abt. Vegetative Physiologie und Pathophysiologie Universit\u00e4tsmedizin G\u00f6ttingen Humboldtallee 23 G\u00f6ttingen 37073 Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Birgitta C.","family":"Burckhardt","sequence":"additional","affiliation":[{"name":"Zentrum Physiologie und Pathophysiologie, Abt. 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