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Regulation of the Fructose Transporter Gene Slc2a5 Expression by Glucose in Cultured Microglial Cells

Tooru M Mizuno1, Pei San Lew1, Gursagar Jhanji1

  • 1Division of Endocrinology and Metabolic Diseases, Department of Physiology & Pathophysiology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R3E 0J9, Canada.

International Journal of Molecular Sciences
|December 10, 2021
PubMed

Insights

High glucose levels activate microglia, impacting metabolism and inflammation. This activation involves the glucose transporter GLUT5 and affects inflammatory gene expression, suggesting a role in metabolic regulation.

Area of Science:

  • Neuroscience
  • Immunology
  • Metabolism

Background:

  • Microglia are key immune cells in the brain involved in metabolism and obesity pathogenesis.
  • Microglial activity is sensitive to dietary and metabolic changes.
  • Solute carrier family 2 member 5 (Slc2a5), encoding glucose transporter 5 (GLUT5), is expressed in microglia but its nutritional regulation is unclear.

Purpose of the Study:

  • To investigate how nutrients, specifically glucose and fructose, regulate microglial activity.
  • To determine the role of glucose transporters, particularly GLUT5, in microglial responses to nutrients.
  • To test the hypothesis that nutrients alter microglial activity by modulating glucose transporter gene expression.

Main Methods:

  • Exposed murine microglial cell line (SIM-A9) and primary microglia to varying glucose concentrations.
  • Measured microglial activation markers (e.g., c-Fos) and glucose transporter gene expression (Slc2a5).
  • Assessed pro-inflammatory cytokine gene expression and effects of GLUT5 inhibition.

Main Results:

  • High glucose concentrations increased c-Fos, Slc2a5 mRNA, and pro-inflammatory cytokine genes in microglia over time.
  • Fructose did not induce similar changes in microglial activation or gene expression.
  • GLUT5 inhibition partially reduced glucose-induced pro-inflammatory gene expression.

Conclusions:

  • Increased local glucose availability activates microglia, influencing their carbohydrate sensing mechanisms.
  • Microglial activation by glucose occurs through both GLUT5-dependent and -independent pathways.
  • These findings highlight a novel mechanism linking glucose metabolism to microglial function and inflammation.
Keywords:
fructoseglucosemicroglianutrientobesity

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