Linked Life Data

6337860

Source:http://linkedlifedata.com/resource/pubmed/id/6337860

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1983-4-15
pubmed:abstractText
The nature of glucose transport at the microvascular blood-retinal barrier was studied using primary cultures of microvascular endothelial cells from bovine retina. Uptake of 3-O-methyl-D-glucose (3MG), a non-metabolizable glucose analogue, was rapid and equilibrative. 3MG uptake could be inhibited by traditional glucose transport inhibitors such as phloretin, phlorizin and cytochalasin B but not by agents that deplete intracellular ATP (2,4-dinitrophenol) or that abolish the sodium gradient (ouabain). Uptake of 3MG by the cells could be stimulated by preloading with 50 mM-glucose, a phenomenon known as counter-transport. Insulin had no effect on 3MG uptake in the cells even after prolonged insulin deprivation. These results demonstrate the existence of a facilitative-diffusion type of glucose transport system in endothelial cells of the retinal microvasculature. Studies with 2-deoxy-D-glucose demonstrated that transport was not rate limiting for metabolism and that the endothelial cells contain free sugar when exposed to an extracellular sugar concentration in the physiologic range. The presence of this free sugar within the cell is necessary for efficient transendothelial transfer of glucose from blood to retina but it could also provide the basis for capillary damage in diabetes mellitus.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0014-4835
pubmed:author
pubmed:issnType
Print
pubmed:volume
36
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
269-77
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
Hexose transport in microvascular endothelial cells cultured from bovine retina.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.