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Myeloid Slc2a1 -Deficient Murine Model Revealed Macrophage Activation and Metabolic Phenotype Are Fueled by GLUT1
Journal article   Peer reviewed

Myeloid Slc2a1 -Deficient Murine Model Revealed Macrophage Activation and Metabolic Phenotype Are Fueled by GLUT1

Alex J Freemerman, Liyang Zhao, Ajeeth K Pingili, Bin Teng, Alyssa J Cozzo, Ashley M Fuller, Amy R Johnson, J Justin Milner, Maili F Lim, Joseph A Galanko, …
The Journal of immunology (1950), Vol.202(4), pp.1265-1286
02/15/2019
DOI: 10.4049/jimmunol.1800002
PMCID: PMC6360258
PMID: 30659108

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Abstract

Macrophages (MΦs) are heterogeneous and metabolically flexible, with metabolism strongly affecting immune activation. A classic response to proinflammatory activation is increased flux through glycolysis with a downregulation of oxidative metabolism, whereas alternative activation is primarily oxidative, which begs the question of whether targeting glucose metabolism is a viable approach to control MΦ activation. We created a murine model of myeloid-specific glucose transporter GLUT1 (
Phenotype Macrophages - metabolism Animals Glucose Transporter Type 1 - deficiency Mice, Inbred C57BL Glucose Transporter Type 1 - metabolism Mice Disease Models, Animal Mice, Knockout

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