Inflammatory cells use glucose as a primary source of metabolic energy, and thus increased uptake of glucose and high rates of glycolysis are characteristics of inflamed cells. Taurine chloramine (TauCl) is the product of a reaction between cellular taurine and hypochlorous acid (HOCl/OCl-), the latter produced by the halide-dependent myeloperoxidase (MPO) system in inflammatory cells. Taurine, a major metabolite of cysteine, protects cells from inflammatory injury by removing toxic hypochlorous acid formed by the MPO system, and also by inhibiting the production of inflammatory mediators. In the present study, we examined the effect of TauCl on glucose uptake and the expression of the glucose transporter 1 (GLUT1) in RAW 264.7 murine macrophages stimulated with lipopolysaccharide (LPS). Glucose uptake was measured by employing labeled glucose analogue [18F]-2-fluoro-2-deoxy-D-glucose (FDG). Stimulation RAW 264.7 cells with LPS increased glucose uptake and led to an upregulation in GLUT1 expression, effects that were abrogated in macrophages treated with TauCl. These data suggest that TauCl can inhibit LPS-mediated enhancement of glucose uptake through inhibition of the upregulation of glucose transporter expression in activated macrophages. This represents one of the mechanisms by which TauCl modulates inflammatory cell function.