{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T20:19:16Z","timestamp":1790799556714,"version":"4.1.0"},"reference-count":127,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2019,2,1]],"date-time":"2019-02-01T00:00:00Z","timestamp":1548979200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,2,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Macrophages (M\u03a6s) 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 M\u03a6 activation. We created a murine model of myeloid-specific glucose transporter GLUT1 (Slc2a1) deletion. Bone marrow\u2013derived M\u03a6s (BMDM) from Slc2a1M\u2212\/\u2212 mice failed to uptake glucose and demonstrated reduced glycolysis and pentose phosphate pathway activity. Activated BMDMs displayed elevated metabolism of oleate and glutamine, yet maximal respiratory capacity was blunted in M\u03a6 lacking GLUT1, demonstrating an incomplete metabolic reprogramming. Slc2a1M\u2212\/\u2212 BMDMs displayed a mixed inflammatory phenotype with reductions of the classically activated pro- and anti-inflammatory markers, yet less oxidative stress. Slc2a1M\u2212\/\u2212 BMDMs had reduced proinflammatory metabolites, whereas metabolites indicative of alternative activation\u2014such as ornithine and polyamines\u2014were greatly elevated in the absence of GLUT1. Adipose tissue M\u03a6s of lean Slc2a1M\u2212\/\u2212 mice had increased alternative M2-like activation marker mannose receptor CD206, yet lack of GLUT1 was not a critical mediator in the development of obesity-associated metabolic dysregulation. However, Ldlr\u2212\/\u2212 mice lacking myeloid GLUT1 developed unstable atherosclerotic lesions. Defective phagocytic capacity in Slc2a1M\u2212\/\u2212 BMDMs may have contributed to unstable atheroma formation. Together, our findings suggest that although lack of GLUT1 blunted glycolysis and the pentose phosphate pathway, M\u03a6 were metabolically flexible enough that inflammatory cytokine release was not dramatically regulated, yet phagocytic defects hindered M\u03a6 function in chronic diseases.<\/jats:p>","DOI":"10.4049\/jimmunol.1800002","type":"journal-article","created":{"date-parts":[[2019,1,18]],"date-time":"2019-01-18T18:05:14Z","timestamp":1547834714000},"page":"1265-1286","source":"Crossref","is-referenced-by-count":133,"title":["Myeloid\n                    <i>Slc2a1<\/i>\n                    -Deficient Murine Model Revealed Macrophage Activation and Metabolic Phenotype Are Fueled by GLUT1"],"prefix":"10.1093","volume":"202","author":[{"given":"Alex J","family":"Freemerman","sequence":"first","affiliation":[{"name":"Department of Nutrition, University of North Carolina at Chapel Hill , Chapel Hill, NC 25799"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1960-0199","authenticated-orcid":false,"given":"Liyang","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Nutrition, University of North Carolina at Chapel Hill , Chapel Hill, NC 25799"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ajeeth K","family":"Pingili","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Tennessee Health Science Center , Memphis, TN 38163"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bin","family":"Teng","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Tennessee Health Science Center , Memphis, TN 38163"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alyssa J","family":"Cozzo","sequence":"additional","affiliation":[{"name":"Department of Nutrition, University of North Carolina at Chapel Hill , Chapel Hill, NC 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