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      Oligodendrocyte Progenitor Cells Directly Utilize Lactate for Promoting Cell Cycling and Differentiation

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          Abstract

          Oligodendrocyte progenitor cells (OPCs) undergo marked morphological changes to become mature oligodendrocytes, but the metabolic resources for this process have not been fully elucidated. Although lactate, a metabolic derivative of glycogen, has been reported to be consumed in oligodendrocytes as a metabolite, and to ameliorate hypomyelination induced by low glucose conditions, it is not clear about the direct contribution of lactate to cell cycling and differentiation of OPCs, and the source of lactate for remyelination. Therefore, we evaluated the effect of 1,4‐dideoxy‐1,4‐imino‐d‐arabinitol (DAB), an inhibitor of the glycogen catabolic enzyme glycogen phosphorylase, in a mouse cuprizone model. Cuprizone induced demyelination in the corpus callosum and remyelination occurred after cuprizone treatment ceased. This remyelination was inhibited by the administration of DAB. To further examine whether lactate affects proliferation or differentiation of OPCs, we cultured mouse primary OPC‐rich cells and analyzed the effect of lactate. Lactate rescued the slowed cell cycling induced by 0.4 mM glucose, as assessed by the BrdU‐positive cell ratio. Lactate also promoted OPC differentiation detected by monitoring the mature oligodendrocyte marker myelin basic protein, in the presence of both 36.6 mM and 0.4 mM glucose. Furthermore, these lactate‐mediated effects were suppressed by the reported monocarboxylate transporter inhibitor, α‐cyano‐4‐hydroxy‐cinnamate. These results suggest that lactate directly promotes the cell cycling rate and differentiation of OPCs, and that glycogen, one of the sources of lactate, contributes to remyelination in vivo. J. Cell. Physiol. 232: 986–995, 2017. © 2016 The Authors. Journal of Cellular Physiology Published by Wiley Periodicals, Inc.

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          Brain energy metabolism: focus on astrocyte-neuron metabolic cooperation.

          The energy requirements of the brain are very high, and tight regulatory mechanisms operate to ensure adequate spatial and temporal delivery of energy substrates in register with neuronal activity. Astrocytes-a type of glial cell-have emerged as active players in brain energy delivery, production, utilization, and storage. Our understanding of neuroenergetics is rapidly evolving from a "neurocentric" view to a more integrated picture involving an intense cooperativity between astrocytes and neurons. This review focuses on the cellular aspects of brain energy metabolism, with a particular emphasis on the metabolic interactions between neurons and astrocytes. Copyright © 2011 Elsevier Inc. All rights reserved.
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            Myelination of the nervous system: mechanisms and functions.

            Myelination of axons in the nervous system of vertebrates enables fast, saltatory impulse propagation, one of the best-understood concepts in neurophysiology. However, it took a long while to recognize the mechanistic complexity both of myelination by oligodendrocytes and Schwann cells and of their cellular interactions. In this review, we highlight recent advances in our understanding of myelin biogenesis, its lifelong plasticity, and the reciprocal interactions of myelinating glia with the axons they ensheath. In the central nervous system, myelination is also stimulated by axonal activity and astrocytes, whereas myelin clearance involves microglia/macrophages. Once myelinated, the long-term integrity of axons depends on glial supply of metabolites and neurotrophic factors. The relevance of this axoglial symbiosis is illustrated in normal brain aging and human myelin diseases, which can be studied in corresponding mouse models. Thus, myelinating cells serve a key role in preserving the connectivity and functions of a healthy nervous system.
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              • Abstract: found
              • Article: not found

              The SLC16 gene family-from monocarboxylate transporters (MCTs) to aromatic amino acid transporters and beyond.

              The monocarboxylate cotransporter (MCT) family now comprises 14 members, of which only the first four (MCT1-MCT4) have been demonstrated experimentally to catalyse the proton-linked transport of metabolically important monocarboxylates such as lactate, pyruvate and ketone bodies. SLC16A10 (T-type amino-acid transporter-1, TAT1) is an aromatic amino acid transporter whilst the other members await characterization. MCTs have 12 transmembrane domains (TMDs) with intracellular N- and C-termini and a large intracellular loop between TMDs 6 and 7. MCT1 and MCT4 require a monotopic ancillary protein, CD147, for expression of functional protein at the plasma membrane. Lactic acid transport across the plasma membrane is fundamental for the metabolism of and pH regulation of all cells, removing lactic acid produced by glycolysis and allowing uptake by those cells utilizing it for gluconeogenesis (liver and kidney) or as a respiratory fuel (heart and red muscle). The properties of the different MCT isoforms and their tissue distribution and regulation reflect these roles.
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                Author and article information

                Contributors
                ogata-toru@rehab.go.jp
                Journal
                J Cell Physiol
                J. Cell. Physiol
                10.1002/(ISSN)1097-4652
                JCP
                Journal of Cellular Physiology
                John Wiley and Sons Inc. (Hoboken )
                0021-9541
                1097-4652
                30 November 2016
                May 2017
                : 232
                : 5 ( doiID: 10.1002/jcp.v232.5 )
                : 986-995
                Affiliations
                [ 1 ] Department of Rehabilitation for Movement FunctionsNational Rehabilitation Center for Persons With Disabilities SaitamaJapan
                Author notes
                [*] [* ] Correspondence to: Toru Ogata, Department of Rehabilitation for Movement Functions, National Rehabilitation Center for Persons With Disabilities, 4‐1 Namiki, Tokorozawa, Saitama 359‐8555, Japan. E‐mail: ogata-toru@ 123456rehab.go.jp

                Article
                JCP25690
                10.1002/jcp.25690
                5299506
                27861886
                90cb53da-6f07-4099-b9af-b75ee96aec93
                © 2016 The Authors. Journal of Cellular Physiology Published by Wiley Periodicals, Inc.

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 21 April 2016
                : 11 November 2016
                Page count
                Figures: 7, Tables: 0, Pages: 10, Words: 7808
                Funding
                Funded by: JSPS KAKENHI from the Ministry of Education, Culture, Sports, Science, and Technology of Japan
                Award ID: 25893291
                Funded by: MEXT
                Award ID: S1511017
                Categories
                Original Research Article
                Original Research Articles
                Custom metadata
                2.0
                jcp25690
                May 2017
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.0.5 mode:remove_FC converted:09.02.2017

                Anatomy & Physiology
                Anatomy & Physiology

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