کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2949749 | 1577253 | 2011 | 12 صفحه PDF | دانلود رایگان |
ObjectivesThis study investigated the regulation of glucose uptake in cells that participate in atherogenesis by stimuli relevant to this process, to gain mechanistic insight into the origin of the 18fluorine-labeled 2-deoxy-D-glucose (FdG) uptake signals observed clinically.BackgroundPatient studies suggest that positron emission tomography (PET) using FdG can detect “active” atherosclerotic plaques, yet the mechanism giving rise to FdG signals remains unknown.MethodsWe exposed cells to conditions thought to operate in atheroma and determined rates of glucose uptake.ResultsHypoxia, but not pro-inflammatory cytokines, potently stimulated glucose uptake in human macrophages and foam cells. Statins attenuated this process in vitro, suggesting that these agents have a direct effect on human macrophages. Immunohistochemical study of human plaques revealed abundant expression of proteins regulating glucose utilization, predominantly in macrophage-rich regions of the plaques—regions previously proved hypoxic. Smooth-muscle cells and endothelial cells markedly increased rates of glucose uptake when exposed to pro-inflammatory cytokines.ConclusionsGlucose uptake and, probably, FdG uptake signals in atheroma may reflect hypoxia-stimulated macrophages rather than mere inflammatory burden. Cytokine-activated smooth-muscle cells also may contribute to the FdG signal.
Journal: Journal of the American College of Cardiology - Volume 58, Issue 6, 2 August 2011, Pages 603–614