ArticlePLoS computational biology2012
Determinants of brain cell metabolic phenotypes and energy substrate utilization unraveled with a modeling approach.
Article in PLoS computational biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- The role of NURR1 in metabolic abnormalities of Parkinson's disease.Molecular neurodegeneration · 2022Review
- The Glioblastoma Microenvironment: Morphology, Metabolism, and Molecular Signature of Glial Dynamics to Discover Metabolic Rewiring Sequence.International journal of molecular sciences · 2021Review
- A Standardized Brain Molecular Atlas: A Resource for Systems Modeling and Simulation.Frontiers in molecular neuroscience · 2021Article
- Thermodynamics in Neurodegenerative Diseases: Interplay Between Canonical WNT/Beta-Catenin Pathway-PPAR Gamma, Energy Metabolism and Circadian Rhythms.Neuromolecular medicine · 2018Review
- Metabolic Pathways of the Warburg Effect in Health and Disease: Perspectives of Choice, Chain or Chance.International journal of molecular sciences · 2017Review
- Multi-timescale modeling of activity-dependent metabolic coupling in the neuron-glia-vasculature ensemble.PLoS computational biology · 2015Article
- Propofol compared with isoflurane inhibits mitochondrial metabolism in immature swine cerebral cortex.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014Article
- Alzheimer's disease: the amyloid hypothesis and the Inverse Warburg effect.Frontiers in physiology · 2014Article
- Lactate oxidation at the mitochondria: a lactate-malate-aspartate shuttle at work.Frontiers in neuroscience · 2014Article
- Unraveling the complex metabolic nature of astrocytes.Frontiers in cellular neuroscience · 2013Review
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
Although all brain cells bear in principle a comparable potential in terms of energetics, in reality they exhibit different metabolic profiles. The specific biochemical characteristics explaining such disparities and their relative importance are largely unknown. Using a modeling approach, we show that modifying the kinetic parameters of pyruvate dehydrogenase and mitochondrial NADH shuttling within a realistic interval can yield a striking switch in lactate flux direction. In this context, cells having essentially an oxidative profile exhibit pronounced extracellular lactate uptake and consumption. However, they can be turned into cells with prominent aerobic glycolysis by selectively reducing the aforementioned parameters. In the case of primarily oxidative cells, we also examined the role of glycolysis and lactate transport in providing pyruvate to mitochondria in order to sustain oxidative phosphorylation. The results show that changes in lactate transport capacity and extracellular lactate concentration within the range described experimentally can sustain enhanced oxidative metabolism upon activation. Such a demonstration provides key elements to understand why certain brain cell types constitutively adopt a particular metabolic profile and how specific features can be altered under different physiological and pathological conditions in order to face evolving energy demands.
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