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

• Published in: International journal of molecular sciences Vol. 22; no. 23; p. 12668
• Main Authors: Mizuno, Tooru M, Lew, Pei San, Jhanji, Gursagar
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 23.11.2021; MDPI
• Subjects: Animals; c-Fos protein; Carbohydrates; Cell activation; Cells, Cultured; Central nervous system; Cytokines; Diet; Food; Fructose; Gene expression; Gene Expression Regulation - drug effects; Genes; Glucose; Glucose - pharmacology; Glucose transporter; Glucose transporter type 5; Glucose Transporter Type 5 - genetics; Hypothalamus; Inflammation; Kinases; Metabolism; Mice; Microglia; Microglia - cytology; Microglia - drug effects; Microglia - metabolism; Microglial cells; Neurons; nutrient; Nutrients; Nutrition; Obesity; Pathogenesis; Proto-Oncogene Proteins c-fos - genetics; fructose; glucose; nutrient; microglia; obesity
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms222312668

Microglia play a role in the regulation of metabolism and pathogenesis of obesity. Microglial activity is altered in response to changes in diet and the body's metabolic state. Solute carrier family 2 member 5 ( ) that encodes glucose transporter 5 (GLUT5) is a fructose transporter primarily expressed in microglia within the central nervous system. However, little is known about the nutritional regulation of expression in microglia and its role in the regulation of metabolism. The present study aimed to address the hypothesis that nutrients affect microglial activity by altering the expression of glucose transporter genes. Murine microglial cell line SIM-A9 cells and primary microglia from mouse brain were exposed to different concentrations of glucose and levels of microglial activation markers and glucose transporter genes were measured. High concentration of glucose increased levels of the immediate-early gene product c-Fos, a marker of cell activation, mRNA, and pro-inflammatory cytokine genes in microglial cells in a time-dependent manner, while fructose failed to cause these changes. Glucose-induced changes in pro-inflammatory gene expression were partially attenuated in SIM-A9 cells treated with the GLUT5 inhibitor. These findings suggest that an increase in local glucose availability leads to the activation of microglia by controlling their carbohydrate sensing mechanism through both GLUT5-dependent and -independent mechanisms.