Contribution of extracellular glutamine as an anaplerotic substrate to neuronal metabolism: a re-evaluation by multinuclear NMR spectroscopy in primary cultured neurons

Multinuclear NMR spectroscopy is used to investigate the effect of glutamine on neuronal glucose metabolism. Primary neurons were incubated with [1-(13C)]glucose in the absence or presence of glutamine (2 mM) and/or NH4Cl (5 mM). After ammonia-treatment, the concentrations of high-energy phosphates...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Neurochemical research 2005-10, Vol.30 (10), p.1269-1281
Hauptverfasser: Shokati, Touraj, Zwingmann, Claudia, Leibfritz, Dieter
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 1281
container_issue 10
container_start_page 1269
container_title Neurochemical research
container_volume 30
creator Shokati, Touraj
Zwingmann, Claudia
Leibfritz, Dieter
description Multinuclear NMR spectroscopy is used to investigate the effect of glutamine on neuronal glucose metabolism. Primary neurons were incubated with [1-(13C)]glucose in the absence or presence of glutamine (2 mM) and/or NH4Cl (5 mM). After ammonia-treatment, the concentrations of high-energy phosphates decreased up to 84% of control, which was aggravated in glutamine-containing medium (up to 42% of control). These effects could not be attributed to changes in mitochondrial glucose oxidation. Withdrawal of glutamine decreased amino acid concentrations, e.g. of glutamate to 53%, but also considerably lessened the 13C enrichment in [4-(13C)]glutamate to 8.3% of control, and decreased the 13C-enrichment in acetyl-CoA entering the Krebs cycle (P < 0.001). Thus, although glutamine is potent in replenishing neuronal glutamate stores, glutamate formation is mainly attributed to its de novo synthesis from glucose. Furthermore, mitochondrial glucose metabolism strongly depends on the supply of carbons from glutamine, indicating that exogenous glutamine is a well-suited substrate to replenish neuronal Krebs cycle intermediates.
doi_str_mv 10.1007/s11064-005-8798-8
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_68887401</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>939706231</sourcerecordid><originalsourceid>FETCH-LOGICAL-c357t-34ea3f3c79fcbdc5b998d175fd6b6a4587dff505a0f855892f2927dd4edbc5fe3</originalsourceid><addsrcrecordid>eNqFkc2q1TAUhYMo3uPVB3AiwYGzatI0TepMDv7BVUF0HNJkR3pJk5of8byRj2mOpyA4EQJ7kG-twfoQekzJc0qIeJEpJePQEcI7KSbZyTvoQLlg3TgRdhcdCGu_jE7kCj3I-ZaQlurpfXRFRzZQLuUB_TrGUNIy17LEgKPD8LMkbcD76nXC33wtel0CYJ2xDu3pzUOKZTE41zk3tgAuEQeoKQbt8QpFz9EveX2JNU7QwQ_tq_5TP5_wWn1ZQjUeWvvHD59x3sCUFLOJ2wkvAW9pWXU6YdPAmsDuzfkhuue0z_Bov9fo65vXX47vuptPb98fX910hnFROjaAZo4ZMTkzW8PnaZKWCu7sOI964FJY5zjhmjjJuZx610-9sHYAOxvugF2jZ5feLcXvFXJR65LPe-gAsWY1SinFQOh_QSr6NjJhDXz6D3gba2pbZdX3VMjmRDSIXiDTtsgJnNqHUJSos2x1ka2abHWWrWTLPNmL67yC_ZvY7bLfaI6qUw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>221780027</pqid></control><display><type>article</type><title>Contribution of extracellular glutamine as an anaplerotic substrate to neuronal metabolism: a re-evaluation by multinuclear NMR spectroscopy in primary cultured neurons</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Shokati, Touraj ; Zwingmann, Claudia ; Leibfritz, Dieter</creator><creatorcontrib>Shokati, Touraj ; Zwingmann, Claudia ; Leibfritz, Dieter</creatorcontrib><description>Multinuclear NMR spectroscopy is used to investigate the effect of glutamine on neuronal glucose metabolism. Primary neurons were incubated with [1-(13C)]glucose in the absence or presence of glutamine (2 mM) and/or NH4Cl (5 mM). After ammonia-treatment, the concentrations of high-energy phosphates decreased up to 84% of control, which was aggravated in glutamine-containing medium (up to 42% of control). These effects could not be attributed to changes in mitochondrial glucose oxidation. Withdrawal of glutamine decreased amino acid concentrations, e.g. of glutamate to 53%, but also considerably lessened the 13C enrichment in [4-(13C)]glutamate to 8.3% of control, and decreased the 13C-enrichment in acetyl-CoA entering the Krebs cycle (P &lt; 0.001). Thus, although glutamine is potent in replenishing neuronal glutamate stores, glutamate formation is mainly attributed to its de novo synthesis from glucose. Furthermore, mitochondrial glucose metabolism strongly depends on the supply of carbons from glutamine, indicating that exogenous glutamine is a well-suited substrate to replenish neuronal Krebs cycle intermediates.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-005-8798-8</identifier><identifier>PMID: 16341588</identifier><language>eng</language><publisher>United States: Springer Nature B.V</publisher><subject>Ammonium Chloride - metabolism ; Animals ; Carbon Radioisotopes - chemistry ; Carbon Radioisotopes - metabolism ; Cells, Cultured ; Citric Acid Cycle - physiology ; Culture Media - chemistry ; Energy Metabolism ; Glucose - chemistry ; Glucose - metabolism ; Glutamine - metabolism ; Neurons - cytology ; Neurons - metabolism ; Nuclear Magnetic Resonance, Biomolecular ; Rats</subject><ispartof>Neurochemical research, 2005-10, Vol.30 (10), p.1269-1281</ispartof><rights>Springer Science+Business Media, Inc. 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c357t-34ea3f3c79fcbdc5b998d175fd6b6a4587dff505a0f855892f2927dd4edbc5fe3</citedby><cites>FETCH-LOGICAL-c357t-34ea3f3c79fcbdc5b998d175fd6b6a4587dff505a0f855892f2927dd4edbc5fe3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27907,27908</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16341588$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shokati, Touraj</creatorcontrib><creatorcontrib>Zwingmann, Claudia</creatorcontrib><creatorcontrib>Leibfritz, Dieter</creatorcontrib><title>Contribution of extracellular glutamine as an anaplerotic substrate to neuronal metabolism: a re-evaluation by multinuclear NMR spectroscopy in primary cultured neurons</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><description>Multinuclear NMR spectroscopy is used to investigate the effect of glutamine on neuronal glucose metabolism. Primary neurons were incubated with [1-(13C)]glucose in the absence or presence of glutamine (2 mM) and/or NH4Cl (5 mM). After ammonia-treatment, the concentrations of high-energy phosphates decreased up to 84% of control, which was aggravated in glutamine-containing medium (up to 42% of control). These effects could not be attributed to changes in mitochondrial glucose oxidation. Withdrawal of glutamine decreased amino acid concentrations, e.g. of glutamate to 53%, but also considerably lessened the 13C enrichment in [4-(13C)]glutamate to 8.3% of control, and decreased the 13C-enrichment in acetyl-CoA entering the Krebs cycle (P &lt; 0.001). Thus, although glutamine is potent in replenishing neuronal glutamate stores, glutamate formation is mainly attributed to its de novo synthesis from glucose. Furthermore, mitochondrial glucose metabolism strongly depends on the supply of carbons from glutamine, indicating that exogenous glutamine is a well-suited substrate to replenish neuronal Krebs cycle intermediates.</description><subject>Ammonium Chloride - metabolism</subject><subject>Animals</subject><subject>Carbon Radioisotopes - chemistry</subject><subject>Carbon Radioisotopes - metabolism</subject><subject>Cells, Cultured</subject><subject>Citric Acid Cycle - physiology</subject><subject>Culture Media - chemistry</subject><subject>Energy Metabolism</subject><subject>Glucose - chemistry</subject><subject>Glucose - metabolism</subject><subject>Glutamine - metabolism</subject><subject>Neurons - cytology</subject><subject>Neurons - metabolism</subject><subject>Nuclear Magnetic Resonance, Biomolecular</subject><subject>Rats</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</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>eNqFkc2q1TAUhYMo3uPVB3AiwYGzatI0TepMDv7BVUF0HNJkR3pJk5of8byRj2mOpyA4EQJ7kG-twfoQekzJc0qIeJEpJePQEcI7KSbZyTvoQLlg3TgRdhcdCGu_jE7kCj3I-ZaQlurpfXRFRzZQLuUB_TrGUNIy17LEgKPD8LMkbcD76nXC33wtel0CYJ2xDu3pzUOKZTE41zk3tgAuEQeoKQbt8QpFz9EveX2JNU7QwQ_tq_5TP5_wWn1ZQjUeWvvHD59x3sCUFLOJ2wkvAW9pWXU6YdPAmsDuzfkhuue0z_Bov9fo65vXX47vuptPb98fX910hnFROjaAZo4ZMTkzW8PnaZKWCu7sOI964FJY5zjhmjjJuZx610-9sHYAOxvugF2jZ5feLcXvFXJR65LPe-gAsWY1SinFQOh_QSr6NjJhDXz6D3gba2pbZdX3VMjmRDSIXiDTtsgJnNqHUJSos2x1ka2abHWWrWTLPNmL67yC_ZvY7bLfaI6qUw</recordid><startdate>200510</startdate><enddate>200510</enddate><creator>Shokati, Touraj</creator><creator>Zwingmann, Claudia</creator><creator>Leibfritz, Dieter</creator><general>Springer Nature B.V</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>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>200510</creationdate><title>Contribution of extracellular glutamine as an anaplerotic substrate to neuronal metabolism: a re-evaluation by multinuclear NMR spectroscopy in primary cultured neurons</title><author>Shokati, Touraj ; Zwingmann, Claudia ; Leibfritz, Dieter</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c357t-34ea3f3c79fcbdc5b998d175fd6b6a4587dff505a0f855892f2927dd4edbc5fe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Ammonium Chloride - metabolism</topic><topic>Animals</topic><topic>Carbon Radioisotopes - chemistry</topic><topic>Carbon Radioisotopes - metabolism</topic><topic>Cells, Cultured</topic><topic>Citric Acid Cycle - physiology</topic><topic>Culture Media - chemistry</topic><topic>Energy Metabolism</topic><topic>Glucose - chemistry</topic><topic>Glucose - metabolism</topic><topic>Glutamine - metabolism</topic><topic>Neurons - cytology</topic><topic>Neurons - metabolism</topic><topic>Nuclear Magnetic Resonance, Biomolecular</topic><topic>Rats</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shokati, Touraj</creatorcontrib><creatorcontrib>Zwingmann, Claudia</creatorcontrib><creatorcontrib>Leibfritz, Dieter</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shokati, Touraj</au><au>Zwingmann, Claudia</au><au>Leibfritz, Dieter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Contribution of extracellular glutamine as an anaplerotic substrate to neuronal metabolism: a re-evaluation by multinuclear NMR spectroscopy in primary cultured neurons</atitle><jtitle>Neurochemical research</jtitle><addtitle>Neurochem Res</addtitle><date>2005-10</date><risdate>2005</risdate><volume>30</volume><issue>10</issue><spage>1269</spage><epage>1281</epage><pages>1269-1281</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>Multinuclear NMR spectroscopy is used to investigate the effect of glutamine on neuronal glucose metabolism. Primary neurons were incubated with [1-(13C)]glucose in the absence or presence of glutamine (2 mM) and/or NH4Cl (5 mM). After ammonia-treatment, the concentrations of high-energy phosphates decreased up to 84% of control, which was aggravated in glutamine-containing medium (up to 42% of control). These effects could not be attributed to changes in mitochondrial glucose oxidation. Withdrawal of glutamine decreased amino acid concentrations, e.g. of glutamate to 53%, but also considerably lessened the 13C enrichment in [4-(13C)]glutamate to 8.3% of control, and decreased the 13C-enrichment in acetyl-CoA entering the Krebs cycle (P &lt; 0.001). Thus, although glutamine is potent in replenishing neuronal glutamate stores, glutamate formation is mainly attributed to its de novo synthesis from glucose. Furthermore, mitochondrial glucose metabolism strongly depends on the supply of carbons from glutamine, indicating that exogenous glutamine is a well-suited substrate to replenish neuronal Krebs cycle intermediates.</abstract><cop>United States</cop><pub>Springer Nature B.V</pub><pmid>16341588</pmid><doi>10.1007/s11064-005-8798-8</doi><tpages>13</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0364-3190
ispartof Neurochemical research, 2005-10, Vol.30 (10), p.1269-1281
issn 0364-3190
1573-6903
language eng
recordid cdi_proquest_miscellaneous_68887401
source MEDLINE; Springer Nature - Complete Springer Journals
subjects Ammonium Chloride - metabolism
Animals
Carbon Radioisotopes - chemistry
Carbon Radioisotopes - metabolism
Cells, Cultured
Citric Acid Cycle - physiology
Culture Media - chemistry
Energy Metabolism
Glucose - chemistry
Glucose - metabolism
Glutamine - metabolism
Neurons - cytology
Neurons - metabolism
Nuclear Magnetic Resonance, Biomolecular
Rats
title Contribution of extracellular glutamine as an anaplerotic substrate to neuronal metabolism: a re-evaluation by multinuclear NMR spectroscopy in primary cultured neurons
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-16T06%3A22%3A28IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Contribution%20of%20extracellular%20glutamine%20as%20an%20anaplerotic%20substrate%20to%20neuronal%20metabolism:%20a%20re-evaluation%20by%20multinuclear%20NMR%20spectroscopy%20in%20primary%20cultured%20neurons&rft.jtitle=Neurochemical%20research&rft.au=Shokati,%20Touraj&rft.date=2005-10&rft.volume=30&rft.issue=10&rft.spage=1269&rft.epage=1281&rft.pages=1269-1281&rft.issn=0364-3190&rft.eissn=1573-6903&rft_id=info:doi/10.1007/s11064-005-8798-8&rft_dat=%3Cproquest_cross%3E939706231%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=221780027&rft_id=info:pmid/16341588&rfr_iscdi=true