pubmed-article:1334411 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1334411 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:1334411 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:1334411 | lifeskim:mentions | umls-concept:C0206131 | lld:lifeskim |
pubmed-article:1334411 | lifeskim:mentions | umls-concept:C0021641 | lld:lifeskim |
pubmed-article:1334411 | lifeskim:mentions | umls-concept:C0001455 | lld:lifeskim |
pubmed-article:1334411 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:1334411 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
pubmed-article:1334411 | lifeskim:mentions | umls-concept:C0439831 | lld:lifeskim |
pubmed-article:1334411 | lifeskim:mentions | umls-concept:C1516240 | lld:lifeskim |
pubmed-article:1334411 | pubmed:dateCreated | 1993-1-8 | lld:pubmed |
pubmed-article:1334411 | pubmed:abstractText | The aim of this study was to characterize further the interaction between cyclic AMP (cAMP) and insulin binding and action. Rat adipocytes were preincubated at 37 degrees C for 20 min, and after energy depletion with KCN, cell-surface 125I-insulin binding was measured. As recently reported [Eriksson, Lönnroth & Smith (1992) Diabetes 41, 707-714], preincubation with insulin rapidly increased the number of cell-surface insulin binding sites up to approximately 5-fold through recruitment within the plasma membrane. This was completely abolished by the presence of 4 mM-N6-monobutyryl cAMP (a non-hydrolysable cAMP analogue) or 1 microM-isoprenaline, without any apparent change in receptor internalization. Insulin-stimulated receptor tyrosine kinase activity was attenuated by the cAMP analogue only if the exposure of the adipocytes was prolonged to 60 min. The cellular sensitivity to insulin, assessed as 3-O-methylglucose uptake, was markedly decreased by the cAMP analogue, and this could be attributed to the impaired cell-surface binding. However, evidence for post-receptor interactions between cAMP and insulin was also found: an impairment of maximal insulin-stimulated 3-O-methylglucose transport and a delay in the rate of activation of the glucose transport system by insulin. In conclusion, these data demonstrate that beta-adrenergic stimulation and elevated cAMP levels markedly impair the ability of insulin to enhance cell-surface insulin-binding capacity. This novel interaction may be an important mechanism for the cellular insensitivity to insulin produced by cAMP. | lld:pubmed |
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pubmed-article:1334411 | pubmed:language | eng | lld:pubmed |
pubmed-article:1334411 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1334411 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:1334411 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:1334411 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1334411 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1334411 | pubmed:month | Dec | lld:pubmed |
pubmed-article:1334411 | pubmed:issn | 0264-6021 | lld:pubmed |
pubmed-article:1334411 | pubmed:author | pubmed-author:SmithUU | lld:pubmed |
pubmed-article:1334411 | pubmed:author | pubmed-author:LönnrothPP | lld:pubmed |
pubmed-article:1334411 | pubmed:author | pubmed-author:ErikssonJ WJW | lld:pubmed |
pubmed-article:1334411 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1334411 | pubmed:day | 1 | lld:pubmed |
pubmed-article:1334411 | pubmed:volume | 288 ( Pt 2) | lld:pubmed |
pubmed-article:1334411 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1334411 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1334411 | pubmed:pagination | 625-9 | lld:pubmed |
pubmed-article:1334411 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:1334411 | pubmed:year | 1992 | lld:pubmed |
pubmed-article:1334411 | pubmed:articleTitle | Cyclic AMP impairs the rapid effect of insulin to enhance cell-surface insulin-binding capacity in rat adipocytes. | lld:pubmed |
pubmed-article:1334411 | pubmed:affiliation | Department of Medicine II, University of Gothenburg, Sahlgren's Hospital, Sweden. | lld:pubmed |
pubmed-article:1334411 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1334411 | pubmed:publicationType | In Vitro | lld:pubmed |
pubmed-article:1334411 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |