期刊
CEREBRAL CORTEX
卷 26, 期 3, 页码 1046-1058出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/cercor/bhu281
关键词
lactate; metabolism; neural progenitors; neurons; PEPCK-M
资金
- Spain's Ministerio de Economia y Competitividad [MAT2011-29778-C02-02, BFU2012-37177]
- European Regional Development Fund
- Generalitat de Catalunya [2009 SGR719]
This study investigated the metabolic requirements for neuronal progenitor maintenance in vitro and in vivo by examining the metabolic adaptations that support neuronal progenitors and neural stem cells (NSCs) in their undifferentiated state. We demonstrate that neuronal progenitors are strictly dependent on lactate metabolism, while glucose induces their neuronal differentiation. Lactate signaling is not by itself capable of maintaining the progenitor phenotype. The consequences of lactate metabolism include increased mitochondrial and oxidative metabolism, with a strict reliance on cataplerosis through the mitochondrial phosphoenolpyruvate carboxykinase (PEPCK-M) pathway to support anabolic functions, such as the production of extracellular matrix. In vivo, lactate maintains/induces populations of postnatal neuronal progenitors/NSCs in a PEPCK-M-dependent manner. Taken together, our data demonstrate that, lactate alone or together with other physical/biochemical cues maintain NSCs/progenitors with a metabolic signature that is classically found in tissues with high anabolic capacity.
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