Linked Life Data

6161802

Source:http://linkedlifedata.com/resource/pubmed/id/6161802

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1981-4-24
pubmed:abstractText
Insulin receptors and several biological effects of insulin were measured in H35 and HTC cells, two rat hepatoma lines in permanent cell culture that have been employed previously to study glucocorticoid action. In H35 cells, insulin at concentrations as low as 1 pM both enhanced tyrosine amino-transferase activity and stimulated [3H]uridine incorporation into RNA. In this cell line, the binding of approximately 10 molecules of insulin/cell was sufficient to elicit these two biological responses. In contrast, in HTC cells, much higher concentrations of insulin (3 nM or greater) were needed to stimulate both tyrosine aminotransferase activity and other biological functions. When insulin receptors were measured, both cell types had a major insulin-binding site with a Kd of approximately 20 nM. H35 cells, however, had approximately 6 times more receptors per cell than HTC cells. In both cell types, insulin degradation was minimal. These findings indicate that several biological functions in H35 cells are extremely sensitive to insulin in vitro. In contrast, HTC cells are much less sensitive to the hormone. This lack of sensitivity in HTC cells most likely reflects a decrease in the number of insulin receptors present. In addition, the very large differences in responsiveness suggest that postreceptor alterations are also operative.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
108
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
44-51
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1981
pubmed:articleTitle
Insulin action in cultured HTC and H35 rat hepatoma cells: receptor binding and hormone sensitivity.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't