Linked Life Data

8323543

Source:http://linkedlifedata.com/resource/pubmed/id/8323543

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-8-5
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
193
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1211-5
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Brief endotoxemia markedly increases expression of GLUT1 glucose transporter in Kupffer, hepatic endothelial and parenchymal cells.
pubmed:affiliation
Department of Physiology, Louisiana State University Medical Center, New Orleans.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.