Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1999-2-22
pubmed:abstractText
Advanced glycation endproducts (AGEs) have been implicated in the pathogenesis of diabetic complications. However, clearance pathways for these products have not been fully delineated. This study investigates changes in AGE binding in the liver in association with experimental diabetes using in vitro and in vivo radioautography techniques. Male Sprague-Dawley rats were randomised into control and diabetic rats and sacrificed after 3 weeks. Frozen liver sections (20 microm) were incubated with 125I-AGE-BSA. To further localise the AGE binding site, in vivo radioautography was performed by injection of 15 microCi of 125I-AGE-BSA into the abdominal aorta of the rat. Specific binding sites for AGEs were detected in the liver by in vitro radioautography. There was a significant increase in 125I-AGE binding in the liver of diabetic rats. Emulsion radioautography revealed that binding was localised primarily in Küpffer and liver endothelial cells. AGE binding sites were increased in the liver after 3 weeks of experimental diabetes. It remains speculative as to whether these binding sites represent AGE clearance receptors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0145-5680
pubmed:author
pubmed:issnType
Print
pubmed:volume
44
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1095-100
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Hepatic advanced glycation endproduct binding is increased in experimental diabetes.
pubmed:affiliation
Department of Medicine, University of Melbourne, Austin and Repatriation Medical Centre, West Heidelberg, Victoria, Australia.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't