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The Strategic Location of Glycogen and Lactate: From Body Energy Reserve to Brain Plasticity
Brain energy metabolism has been the object of intense research in recent years. Pioneering work has identified the different cell types involved in energy production and use. Recent evidence has demonstrated a key role of L-Lactate in brain energy metabolism, producing a paradigm-shift in our under...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2019
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6415680/ https://www.ncbi.nlm.nih.gov/pubmed/30894801 http://dx.doi.org/10.3389/fncel.2019.00082 |
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author | Calì, Corrado Tauffenberger, Arnaud Magistretti, Pierre |
author_facet | Calì, Corrado Tauffenberger, Arnaud Magistretti, Pierre |
author_sort | Calì, Corrado |
collection | PubMed |
description | Brain energy metabolism has been the object of intense research in recent years. Pioneering work has identified the different cell types involved in energy production and use. Recent evidence has demonstrated a key role of L-Lactate in brain energy metabolism, producing a paradigm-shift in our understanding of the neuronal energy metabolism. At the center of this shift, is the identification of a central role of astrocytes in neuroenergetics. Thanks to their morphological characteristics, they are poised to take up glucose from the circulation and deliver energy substrates to neurons. Astrocyte neuron lactate shuttle (ANLS) model, has shown that the main energy substrate that astrocytes deliver to neurons is L-Lactate, to sustain neuronal oxidative metabolism. L-Lactate can also be produced from glycogen, the storage form of glucose, which is exclusively localized in astrocytes. Inhibition of glycogen metabolism and the ensuing inhibition of L-Lactate production leads to cognitive dysfunction. Experimental evidence indicates that the role of lactate in cognitive function relates not only to its role as a metabolic substrate for neurons but also as a signaling molecule for synaptic plasticity. Interestingly, a similar metabolic uncoupling appears to exist in peripheral tissues plasma, whereby glucose provides L-Lactate as the substrate for cellular oxidative metabolism. In this perspective article, we review the known information on the distribution of glycogen and lactate within brain cells, and how this distribution relates to the energy regime of glial vs. neuronal cells. |
format | Online Article Text |
id | pubmed-6415680 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-64156802019-03-20 The Strategic Location of Glycogen and Lactate: From Body Energy Reserve to Brain Plasticity Calì, Corrado Tauffenberger, Arnaud Magistretti, Pierre Front Cell Neurosci Neuroscience Brain energy metabolism has been the object of intense research in recent years. Pioneering work has identified the different cell types involved in energy production and use. Recent evidence has demonstrated a key role of L-Lactate in brain energy metabolism, producing a paradigm-shift in our understanding of the neuronal energy metabolism. At the center of this shift, is the identification of a central role of astrocytes in neuroenergetics. Thanks to their morphological characteristics, they are poised to take up glucose from the circulation and deliver energy substrates to neurons. Astrocyte neuron lactate shuttle (ANLS) model, has shown that the main energy substrate that astrocytes deliver to neurons is L-Lactate, to sustain neuronal oxidative metabolism. L-Lactate can also be produced from glycogen, the storage form of glucose, which is exclusively localized in astrocytes. Inhibition of glycogen metabolism and the ensuing inhibition of L-Lactate production leads to cognitive dysfunction. Experimental evidence indicates that the role of lactate in cognitive function relates not only to its role as a metabolic substrate for neurons but also as a signaling molecule for synaptic plasticity. Interestingly, a similar metabolic uncoupling appears to exist in peripheral tissues plasma, whereby glucose provides L-Lactate as the substrate for cellular oxidative metabolism. In this perspective article, we review the known information on the distribution of glycogen and lactate within brain cells, and how this distribution relates to the energy regime of glial vs. neuronal cells. Frontiers Media S.A. 2019-03-06 /pmc/articles/PMC6415680/ /pubmed/30894801 http://dx.doi.org/10.3389/fncel.2019.00082 Text en Copyright © 2019 Calì, Tauffenberger and Magistretti. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Calì, Corrado Tauffenberger, Arnaud Magistretti, Pierre The Strategic Location of Glycogen and Lactate: From Body Energy Reserve to Brain Plasticity |
title | The Strategic Location of Glycogen and Lactate: From Body Energy Reserve to Brain Plasticity |
title_full | The Strategic Location of Glycogen and Lactate: From Body Energy Reserve to Brain Plasticity |
title_fullStr | The Strategic Location of Glycogen and Lactate: From Body Energy Reserve to Brain Plasticity |
title_full_unstemmed | The Strategic Location of Glycogen and Lactate: From Body Energy Reserve to Brain Plasticity |
title_short | The Strategic Location of Glycogen and Lactate: From Body Energy Reserve to Brain Plasticity |
title_sort | strategic location of glycogen and lactate: from body energy reserve to brain plasticity |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6415680/ https://www.ncbi.nlm.nih.gov/pubmed/30894801 http://dx.doi.org/10.3389/fncel.2019.00082 |
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