Linked Life Data

7033268

Source:http://linkedlifedata.com/resource/pubmed/id/7033268

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1982-3-13
pubmed:abstractText
Insulin stimulation of 2-deoxyglucose uptake in cultured human skin fibroblasts has been examined in the presence of varying concentrations of extracellular glucose. When cell monolayers were preincubated in glucose-free medium, insulin stimulation of hexose transport was small. Increasing glucose levels from 2.7 to 16.7 mM in the preincubation medium enhanced insulin-stimulation 2-deoxyglucose uptake (18-65% of basal uptake). Insulin stimulation of hexose transport in the presence of glucose was the result of an increase in the Vmax without a significant change in the Km of transport. Maximum enhancement of insulin action was achieved 18-24 h after glucose exposure. After 24 h, the insulin response decreased. Glucose did not influence the concentration of insulin required for half-maximal stimulation. Growth conditions also altered the magnitude of insulin stimulation of 2-deoxyglucose uptake; the response was maximal in confluent cells (5-10 days of culture) and decreased during senescence. These data demonstrate that extracellular glucose levels influence insulin action in cultured fibroblasts. This implies that insulin responsiveness in vivo may be regulated in some systems by ambient glucose levels.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0021-972X
pubmed:author
pubmed:issnType
Print
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
34-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
Glucose enhancement of insulin action: elevated glucose levels increase insulin stimulation of 2-deoxyglucose uptake in cultured human fibroblasts.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.