The Role of Lactate in the Central Nervous System and Its Relationship with Related Diseases / 中国生物化学与分子生物学报
Chinese Journal of Biochemistry and Molecular Biology
; (12): 418-423, 2022.
Article
in Zh
| WPRIM
| ID: wpr-1015718
Responsible library:
WPRO
ABSTRACT
Lactate has always been regarded as a metabolic waste in the brain‚ and the understanding of its functions have been seriously lagging behind. In recent years‚ more and more experimental evidence has shown that lactate plays an important role in a variety of physiological and pathological processes. Among nerve cells‚ astrocytes are the main source of cells for the production and release of lactate. The cells produce lactate through aerobic glycolysis‚ which is then released to the outside of the cells via transmembrane channels and enters neurons to supply energy. In the central nervous system‚ lactate plays a significant role in homeostasis regulation. Lactate regulates the functions and activities of neurons mainly through two pathways: metabolic pathways (as energy substrates) and signal pathways (as signal molecules) ‚which is extensively manifested in the regulation of physiological processes such as neuronal energy metabolism‚ excitatory‚ plasticity‚ learning and memory‚ and nervous system development‚ as well as the pathological processes including depression‚ Alzheimer’ s disease (AD) and brain injury. There is a lactate-specific receptor (GPR81) in brain tissue‚ and lactate binds to it to regulate the intracellular second messenger. In addition‚ it was also found that lactate can modulate the excitability of neurons through unknown receptors and other functions as signal molecules. Therefore‚ this article focus on the research progress of lactate as an energy substrate and signaling molecule and its involvement in related neurological diseases‚ which may provide new ideas for the prevention and treatment of related central nervous system diseases.
Full text:
1
Database:
WPRIM
Language:
Zh
Journal:
Chinese Journal of Biochemistry and Molecular Biology
Year:
2022
Document type:
Article