Glutamate Impairs Mitochondria Aerobic Respiration Capacity and Enhances Glycolysis in Cultured Rat Astrocytes

Xu YAN, Zhong Fang SHI, Li Xin XU, Jia Xin LI, Min WU, Xiao Xuan WANG, Mei JIA, Li Ping DONG, Shaohua Yang, Fang YUAN

Research output: Contribution to journalArticleResearchpeer-review

9 Citations (Scopus)

Abstract

Objective To study the effect of glutamate on metabolism, shifts in glycolysis and lactate release in rat astrocytes. Methods After 10 days, secondary cultured astrocytes were treated with 1 mmol/L glutamate for 1 h, and the oxygen consumption rates (OCR) and extra cellular acidification rate (ECAR) was analyzed using a Seahorse XF 24 Extracellular Flux Analyzer. Cell viability was then evaluated by MTT assay. Moreover, changes in extracellular lactate concentration induced by glutamate were tested with a lactate detection kit. Results Compared with the control group, treatment with 1 mmol/L glutamate decreased the astrocytes' maximal respiration and spare respiratory capacity but increased their glycolytic capacity and glycolytic reserve. Further analysis found that 1-h treatment with different concentrations of glutamate (0.1-1 mmol/L) increased lactate release from astrocytes, however the cell viability was not affected by the glutamate treatment. Conclusion The current study provided direct evidence that exogenous glutamate treatment impaired the mitochondrial respiration capacity of astrocytes and enhanced aerobic glycolysis, which could be involved in glutamate injury or protection mechanisms in response to neurological disorders.

Original languageEnglish
Pages (from-to)44-51
Number of pages8
JournalBiomedical and Environmental Sciences
Volume30
Issue number1
DOIs
StatePublished - 1 Jan 2017

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Glycolysis
Astrocytes
Glutamic Acid
Mitochondria
Respiration
Lactic Acid
Cell Survival
Smegmamorpha
Nervous System Diseases
Oxygen Consumption
Control Groups
Wounds and Injuries

Keywords

  • Astrocytes
  • Glutamate
  • Glycolysis
  • Lactate
  • Mitochondrial metabolism

Cite this

YAN, Xu ; SHI, Zhong Fang ; XU, Li Xin ; LI, Jia Xin ; WU, Min ; WANG, Xiao Xuan ; JIA, Mei ; DONG, Li Ping ; Yang, Shaohua ; YUAN, Fang. / Glutamate Impairs Mitochondria Aerobic Respiration Capacity and Enhances Glycolysis in Cultured Rat Astrocytes. In: Biomedical and Environmental Sciences. 2017 ; Vol. 30, No. 1. pp. 44-51.
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abstract = "Objective To study the effect of glutamate on metabolism, shifts in glycolysis and lactate release in rat astrocytes. Methods After 10 days, secondary cultured astrocytes were treated with 1 mmol/L glutamate for 1 h, and the oxygen consumption rates (OCR) and extra cellular acidification rate (ECAR) was analyzed using a Seahorse XF 24 Extracellular Flux Analyzer. Cell viability was then evaluated by MTT assay. Moreover, changes in extracellular lactate concentration induced by glutamate were tested with a lactate detection kit. Results Compared with the control group, treatment with 1 mmol/L glutamate decreased the astrocytes' maximal respiration and spare respiratory capacity but increased their glycolytic capacity and glycolytic reserve. Further analysis found that 1-h treatment with different concentrations of glutamate (0.1-1 mmol/L) increased lactate release from astrocytes, however the cell viability was not affected by the glutamate treatment. Conclusion The current study provided direct evidence that exogenous glutamate treatment impaired the mitochondrial respiration capacity of astrocytes and enhanced aerobic glycolysis, which could be involved in glutamate injury or protection mechanisms in response to neurological disorders.",
keywords = "Astrocytes, Glutamate, Glycolysis, Lactate, Mitochondrial metabolism",
author = "Xu YAN and SHI, {Zhong Fang} and XU, {Li Xin} and LI, {Jia Xin} and Min WU and WANG, {Xiao Xuan} and Mei JIA and DONG, {Li Ping} and Shaohua Yang and Fang YUAN",
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Glutamate Impairs Mitochondria Aerobic Respiration Capacity and Enhances Glycolysis in Cultured Rat Astrocytes. / YAN, Xu; SHI, Zhong Fang; XU, Li Xin; LI, Jia Xin; WU, Min; WANG, Xiao Xuan; JIA, Mei; DONG, Li Ping; Yang, Shaohua; YUAN, Fang.

In: Biomedical and Environmental Sciences, Vol. 30, No. 1, 01.01.2017, p. 44-51.

Research output: Contribution to journalArticleResearchpeer-review

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AU - YAN, Xu

AU - SHI, Zhong Fang

AU - XU, Li Xin

AU - LI, Jia Xin

AU - WU, Min

AU - WANG, Xiao Xuan

AU - JIA, Mei

AU - DONG, Li Ping

AU - Yang, Shaohua

AU - YUAN, Fang

PY - 2017/1/1

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N2 - Objective To study the effect of glutamate on metabolism, shifts in glycolysis and lactate release in rat astrocytes. Methods After 10 days, secondary cultured astrocytes were treated with 1 mmol/L glutamate for 1 h, and the oxygen consumption rates (OCR) and extra cellular acidification rate (ECAR) was analyzed using a Seahorse XF 24 Extracellular Flux Analyzer. Cell viability was then evaluated by MTT assay. Moreover, changes in extracellular lactate concentration induced by glutamate were tested with a lactate detection kit. Results Compared with the control group, treatment with 1 mmol/L glutamate decreased the astrocytes' maximal respiration and spare respiratory capacity but increased their glycolytic capacity and glycolytic reserve. Further analysis found that 1-h treatment with different concentrations of glutamate (0.1-1 mmol/L) increased lactate release from astrocytes, however the cell viability was not affected by the glutamate treatment. Conclusion The current study provided direct evidence that exogenous glutamate treatment impaired the mitochondrial respiration capacity of astrocytes and enhanced aerobic glycolysis, which could be involved in glutamate injury or protection mechanisms in response to neurological disorders.

AB - Objective To study the effect of glutamate on metabolism, shifts in glycolysis and lactate release in rat astrocytes. Methods After 10 days, secondary cultured astrocytes were treated with 1 mmol/L glutamate for 1 h, and the oxygen consumption rates (OCR) and extra cellular acidification rate (ECAR) was analyzed using a Seahorse XF 24 Extracellular Flux Analyzer. Cell viability was then evaluated by MTT assay. Moreover, changes in extracellular lactate concentration induced by glutamate were tested with a lactate detection kit. Results Compared with the control group, treatment with 1 mmol/L glutamate decreased the astrocytes' maximal respiration and spare respiratory capacity but increased their glycolytic capacity and glycolytic reserve. Further analysis found that 1-h treatment with different concentrations of glutamate (0.1-1 mmol/L) increased lactate release from astrocytes, however the cell viability was not affected by the glutamate treatment. Conclusion The current study provided direct evidence that exogenous glutamate treatment impaired the mitochondrial respiration capacity of astrocytes and enhanced aerobic glycolysis, which could be involved in glutamate injury or protection mechanisms in response to neurological disorders.

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