Nuclear factor kappa B (NFκB) induces insulin resistance in mammals, possibly representing a counter-regulatory response by which the host escapes NFκB-induced hypoglycemia. However, the underlying mechanism remains unclear. To identify the mechanism of NFκB-induced hypoglycemia, we measured hepatocyte glucose production and whole-body glucose utilization in mice. Inhibition of glucose production and utilization by lipopolysaccharide depended on toll-like receptor 4, myeloid differentiation factor 88 and NFκB, while tumor necrosis factor alpha and the insulin signaling intermediate phosphatidylinositol 3-kinase were unnecessary. Taxol, a widely-used cancer drug, also activates toll-like receptor 4 and several of its downstream intermediates, but its mechanism is unclear. To determine whether Taxol destroys tumors by decreasing glucose availability, we measured glucose utilization in vitro. Taxol decreased glucose utilization in MCF7 cells. Additionally, Taxol increased plasma adiponectin, a biomarker of low fasting glucose utilization, in treatment-responsive breast cancer patients. This biomarker could predict the effectiveness of Taxol in individuals.