Brief endotoxemia markedly increases expression of GLUT1 glucose transporter in Kupffer, hepatic endothelial and parenchymal cells.
Brief endotoxemia markedly increases expression of GLUT1 glucose transporter in Kupffer, hepatic endothelial and parenchymal cells.
复制标题
短暂的内毒素血症显着增加库普弗细胞、肝内皮细胞和实质细胞中 GLUT1 葡萄糖转运蛋白的表达。
DOI：
10.1006/bbrc.1993.1754
复制
发表时间：
1993
影响因子：
3.1
通讯作者：
Spitzer,JJ
中科院分区：
文献类型：
--
作者：
Spolarics,Z;Pekala,PH;Bagby,GJ;Spitzer,JJ
Expression of various glucose transporter isoforms was studied in hepatic cells from fasted rats 3h after an injection ofE. coliLPS (1mg/kg bw., iv.). 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 detectible. 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.
