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Publication

Testing the role of myeloid cell glucose flux in inflammation and atherosclerosis.

Authors Nishizawa T, Kanter JE, Kramer F, Barnhart S, Shen X, Vivekanandan-Giri A, Wall VZ, Kowitz J, Devaraj S, O'Brien KD, Pennathur S, Tang J, Miyaoka RS, Raines EW, Bornfeldt KE Submitted By Submitted Externally on 5/2/2014 Status Published Journal Cell reports Year 2014 Date Published 4/24/2014 Volume : Pages 7 : 356 - 365 PubMed Reference Abstract Inflammatory activation of myeloid cells is accompanied by increased glycolysis, which is required for the聽surge in cytokine production. Although in聽vitro studies suggest that increased macrophage glucose metabolism is sufficient for cytokine induction, the proinflammatory effects of increased myeloid cell glucose flux in聽vivo and the impact on atherosclerosis, a major complication of diabetes, are unknown. We therefore tested the hypothesis that increased glucose uptake in myeloid cells stimulates cytokine production and atherosclerosis. Overexpression of the glucose transporter GLUT1 in myeloid cells caused increased glycolysis and flux through the pentose phosphate pathway but did not induce cytokines. Moreover, myeloid-cell-specific overexpression of GLUT1 in LDL receptor-deficient mice was ineffective in promoting atherosclerosis. Thus, increased glucose flux is insufficient for inflammatory myeloid cell activation and atherogenesis. If glucose promotes atherosclerosis by increasing cellular glucose flux, myeloid cells do not appear to be the key targets.

Investigators with authorship
Name Institution Kevin O'Brien University of Washington

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