Hypoglycemia occurs without hyperinsulinemia in suckling rats with endotoxic shock. However, tissue glucose uptake during endotoxic shock is not well known in the newborn. GLUT1 is insulin insensitive and is the predominant glucose transporter in 10 day old rats. In the adult with endotoxic shock, noninsulin-mediated glucose uptake and GLUT1 gene expression increase. Therefore, we hypothesized that tissue glucose uptake and GLUT1 mRNA abundance increased in 10 day old rats with endotoxic shock. The present study showed that whole body glucose disposal increased 3 h after a Salmonella enteritidis lipopolysaccharide injection (LD90 at 72 h). Plasma insulin concentration was not altered. Tissue glucose uptake increased in liver (2.4-fold) and fat (2.6-fold). However, changes of GLUT1 protein concentration were not detected in liver. GLUT1 mRNA abundance increased in liver (9-fold) and fat (4-fold). GLUT1 mRNA abundance but not glucose uptake increased in muscle. Neither glucose uptake or GLUT1 mRNA abundance was altered in brain. The mRNA abundance of tissue-specific glucose transporters (GLUT2 and GLUT4) was not altered. Thus, tissue glucose uptake and GLUT1 mRNA abundance increased without hyperinsulinemia during endotoxic shock in 10 day old rats.