We are analyzing https://link.springer.com/article/10.1007/s11306-010-0208-9.

Title:
Stable isotope-resolved metabolomic analysis of lithium effects on glial-neuronal metabolism and interactions | Metabolomics
Description:
Despite the long-established therapeutic efficacy of lithium in the treatment of bipolar disorder (BPD), its molecular mechanism of action remains elusive. Newly developed stable isotope-resolved metabolomics (SIRM) is a powerful approach that can be used to elucidate systematically how lithium impacts glial and neuronal metabolic pathways and activities, leading ultimately to deciphering its molecular mechanism of action. The effect of lithium on the metabolism of three different 13C-labeled precursors ([U-13C]-glucose, 13C-3-lactate or 13C-2,3-alanine) was analyzed in cultured rat astrocytes and neurons by nuclear magnetic resonance (NMR) spectroscopy and gas chromatography mass spectrometry (GC-MS). Using [U-13C]-glucose, lithium was shown to enhance glycolytic activity and part of the Krebs cycle activity in both astrocytes and neurons, particularly the anaplerotic pyruvate carboxylation (PC). The PC pathway was previously thought to be active in astrocytes but absent in neurons. Lithium also stimulated the extracellular release of 13C labeled-lactate, -alanine (Ala), -citrate, and -glutamine (Gln) by astrocytes. Interrogation of neuronal pathways using 13C-3-lactate or 13C-2,3-Ala as tracers indicated a high capacity of neurons to utilize lactate and Ala in the Krebs cycle, particularly in the production of labeled Asp and Glu via PC and normal cycle activity. Prolonged lithium treatment enhanced lactate metabolism via PC but inhibited lactate oxidation via the normal Krebs cycle in neurons. Such lithium modulation of glycolytic, PC and Krebs cycle activity in astrocytes and neurons as well as release of fuel substrates by astrocytes should help replenish Krebs cycle substrates for Glu synthesis while meeting neuronal demands for energy. Further investigations into the molecular regulation of these metabolic traits should provide new insights into the pathophysiology of mood disorders and early diagnostic markers, as well as new target(s) for effective therapies.
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article, google, scholar, cas, pubmed, lithium, metabolism, journal, brain, fan, metabolomics, astrocytes, molecular, effects, lane, glucose, analysis, higashi, neurons, manji, nmr, cerebral, metabolic, rat, spectroscopy, energy, chen, kaddurahdaouk, lactate, psychiatry, research, disorder, neuronal, regulation, vivo, blood, flow, louisville, usa, stable, metabolomic, magnetic, resonance, cycle, cancer, center, privacy, cookies, content, teresa,

Topics {✒️}

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Lithium at 50: have the neuroprotective effects of this unique cation been overlooked?

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WebPage:
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         headline:Stable isotope-resolved metabolomic analysis of lithium effects on glial-neuronal metabolism and interactions
         description:Despite the long-established therapeutic efficacy of lithium in the treatment of bipolar disorder (BPD), its molecular mechanism of action remains elusive. Newly developed stable isotope-resolved metabolomics (SIRM) is a powerful approach that can be used to elucidate systematically how lithium impacts glial and neuronal metabolic pathways and activities, leading ultimately to deciphering its molecular mechanism of action. The effect of lithium on the metabolism of three different 13C-labeled precursors ([U-13C]-glucose, 13C-3-lactate or 13C-2,3-alanine) was analyzed in cultured rat astrocytes and neurons by nuclear magnetic resonance (NMR) spectroscopy and gas chromatography mass spectrometry (GC-MS). Using [U-13C]-glucose, lithium was shown to enhance glycolytic activity and part of the Krebs cycle activity in both astrocytes and neurons, particularly the anaplerotic pyruvate carboxylation (PC). The PC pathway was previously thought to be active in astrocytes but absent in neurons. Lithium also stimulated the extracellular release of 13C labeled-lactate, -alanine (Ala), -citrate, and -glutamine (Gln) by astrocytes. Interrogation of neuronal pathways using 13C-3-lactate or 13C-2,3-Ala as tracers indicated a high capacity of neurons to utilize lactate and Ala in the Krebs cycle, particularly in the production of labeled Asp and Glu via PC and normal cycle activity. Prolonged lithium treatment enhanced lactate metabolism via PC but inhibited lactate oxidation via the normal Krebs cycle in neurons. Such lithium modulation of glycolytic, PC and Krebs cycle activity in astrocytes and neurons as well as release of fuel substrates by astrocytes should help replenish Krebs cycle substrates for Glu synthesis while meeting neuronal demands for energy. Further investigations into the molecular regulation of these metabolic traits should provide new insights into the pathophysiology of mood disorders and early diagnostic markers, as well as new target(s) for effective therapies.
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      description:Despite the long-established therapeutic efficacy of lithium in the treatment of bipolar disorder (BPD), its molecular mechanism of action remains elusive. Newly developed stable isotope-resolved metabolomics (SIRM) is a powerful approach that can be used to elucidate systematically how lithium impacts glial and neuronal metabolic pathways and activities, leading ultimately to deciphering its molecular mechanism of action. The effect of lithium on the metabolism of three different 13C-labeled precursors ([U-13C]-glucose, 13C-3-lactate or 13C-2,3-alanine) was analyzed in cultured rat astrocytes and neurons by nuclear magnetic resonance (NMR) spectroscopy and gas chromatography mass spectrometry (GC-MS). Using [U-13C]-glucose, lithium was shown to enhance glycolytic activity and part of the Krebs cycle activity in both astrocytes and neurons, particularly the anaplerotic pyruvate carboxylation (PC). The PC pathway was previously thought to be active in astrocytes but absent in neurons. Lithium also stimulated the extracellular release of 13C labeled-lactate, -alanine (Ala), -citrate, and -glutamine (Gln) by astrocytes. Interrogation of neuronal pathways using 13C-3-lactate or 13C-2,3-Ala as tracers indicated a high capacity of neurons to utilize lactate and Ala in the Krebs cycle, particularly in the production of labeled Asp and Glu via PC and normal cycle activity. Prolonged lithium treatment enhanced lactate metabolism via PC but inhibited lactate oxidation via the normal Krebs cycle in neurons. Such lithium modulation of glycolytic, PC and Krebs cycle activity in astrocytes and neurons as well as release of fuel substrates by astrocytes should help replenish Krebs cycle substrates for Glu synthesis while meeting neuronal demands for energy. Further investigations into the molecular regulation of these metabolic traits should provide new insights into the pathophysiology of mood disorders and early diagnostic markers, as well as new target(s) for effective therapies.
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      name:Rima Kaddurah-Daouk
      affiliation:
            name:Duke University Medical Center
            address:
               name:Department of Psychiatry, Duke University Medical Center, Durham, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Chemistry, Center for Regulatory and Environmental Analytical Metabolomics, University of Louisville, Louisville, USA
      name:Department of Medicine, Structural Biology Program, James Graham Brown Cancer Center, University of Louisville, Louisville, USA
      name:Department of Chemistry, University of Louisville, Louisville, USA
      name:Biomarker Laboratory, Laboratory of Molecular Pathophysiology, Mood and Anxiety Disorder Program, National Institute of Mental Health, NIH, Bethesda, USA
      name:Department of Chemistry, Center for Regulatory and Environmental Analytical Metabolomics, University of Louisville, Louisville, USA
      name:Department of Medicine, Structural Biology Program, James Graham Brown Cancer Center, University of Louisville, Louisville, USA
      name:Department of Chemistry, Center for Regulatory and Environmental Analytical Metabolomics, University of Louisville, Louisville, USA
      name:Department of Medicine, Structural Biology Program, James Graham Brown Cancer Center, University of Louisville, Louisville, USA
      name:Biomarker Laboratory, Laboratory of Molecular Pathophysiology, Mood and Anxiety Disorder Program, National Institute of Mental Health, NIH, Bethesda, USA
      name:Biomarker Laboratory, Laboratory of Molecular Pathophysiology, Mood and Anxiety Disorder Program, National Institute of Mental Health, NIH, Bethesda, USA
      name:Biomarker Laboratory, Laboratory of Molecular Pathophysiology, Mood and Anxiety Disorder Program, National Institute of Mental Health, NIH, Bethesda, USA
      name:Biomarker Laboratory, Laboratory of Molecular Pathophysiology, Mood and Anxiety Disorder Program, National Institute of Mental Health, NIH, Bethesda, USA
      name:Biomarker Laboratory, Laboratory of Molecular Pathophysiology, Mood and Anxiety Disorder Program, National Institute of Mental Health, NIH, Bethesda, USA
      name:Biomarker Laboratory, Laboratory of Molecular Pathophysiology, Mood and Anxiety Disorder Program, National Institute of Mental Health, NIH, Bethesda, USA
      name:Johnson & Johnson, Titusville, USA
      name:Department of Psychiatry, Duke University Medical Center, Durham, USA
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