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Related Concept Videos

Glucose Homeostasis: Regulation of Blood Glucose01:02

Glucose Homeostasis: Regulation of Blood Glucose

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Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
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Related Experiment Video

Updated: Oct 18, 2025

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
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Glucose availability limits microglial nitric oxide production.

Erika Castillo1,2, Ebony Mocanu1,2, Gӧkhan Uruk1,2

  • 1Department of Neurology, University of California San Francisco, San Francisco, California, USA.

Journal of Neurochemistry
|September 29, 2021
PubMed
Summary
This summary is machine-generated.

Glucose availability is critical for microglial nitric oxide (NO) production, essential for brain inflammation. Low glucose levels significantly impair NO synthesis, impacting immune responses in the central nervous system.

Keywords:
NADPHabscesshyperglycemiaiNOSpentose phosphate pathway

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Area of Science:

  • Neuroscience
  • Immunology
  • Metabolism

Background:

  • Metabolic intermediates fuel pro-inflammatory molecule production, including nitric oxide (NO).
  • Microglial NO synthesis relies on NADPH, regenerated via the hexose monophosphate shunt (HMP), which uses glucose.
  • Glucose availability may limit microglial NO production.

Purpose of the Study:

  • To investigate the impact of glucose concentration on microglial NO production.
  • To determine the role of the hexose monophosphate shunt in NO synthesis.

Main Methods:

  • Cultured astrocytes and microglia were stimulated with lipopolysaccharide and interferon-γ.
  • Nitric oxide production was measured at varying glucose concentrations.
  • The effect of hexose monophosphate shunt inhibition (6-aminonicotinamide) and metabolic support (malate, NADPH) was assessed.

Main Results:

  • Microglia, but not astrocytes, produced increased NO upon stimulation.
  • NO production was significantly reduced below 0.5 mM glucose.
  • Inhibition of the hexose monophosphate shunt reduced NO production.
  • Malate and NADPH partially restored NO production under glucose deprivation.

Conclusions:

  • The hexose monophosphate shunt is crucial for fueling microglial NO synthesis.
  • Microglial NO production can be limited by glucose availability in the brain, particularly in conditions like infections.