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Biochem Biophys Res Commun. 1993 Jun 30;193(3):1211-5.

Brief endotoxemia markedly increases expression of GLUT1 glucose transporter in Kupffer, hepatic endothelial and parenchymal cells.

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Department of Physiology, Louisiana State University Medical Center, New Orleans.


Expression of various glucose transporter isoforms was studied in hepatic cells from fasted rats 3h after an injection of E. coli LPS (1mg/kg bw., i.v.). Glucose transporter isoform content of plasma membranes from hepatic cells was determined by western blot analysis using polyclonal antibodies. The predominant glucose transporter isoform expressed in parenchymal cells was GLUT2. GLUTS-1 and -4 were also observed to be present; however, GLUT4 protein was expressed to a relatively minor extent. GLUT3 was not detectable. LPS injection resulted in a 50% decrease in GLUT2 while GLUT1 protein doubled. GLUT4 was not altered after LPS. In the plasma membranes of Kupffer and endothelial cells only the GLUT1 isoform was detected. LPS treatment resulted in a 7- and 4-fold increase in the GLUT1 protein content in these cells. These data indicate that the predominant glucose transporter of hepatic nonparenchymal cells is the GLUT1 isoform and its synthesis and/or membrane translocation is augmented in response to LPS. The observed alterations in the contents of glucose transporters indicate adaptive changes to endotoxemia in the glucose consuming and glucose producing populations of hepatic cells.

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