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Cyclic AMP impairs ...
Cyclic AMP impairs the rapid effect of insulin to enhance cell-surface insulin-binding capacity in rat adipocytes
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- Eriksson, Jan W (author)
- Department of Medicine II, University of Gothenburg, Sahlgren's Hospital, Sweden.
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- Lönnroth, P (author)
- Department of Medicine II, University of Gothenburg, Sahlgren's Hospital, Sweden.
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- Smith, U (author)
- Department of Medicine II, University of Gothenburg, Sahlgren's Hospital, Sweden.
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Department of Medicine II, University of Gothenburg, Sahlgren's Hospital, Sweden (creator_code:org_t)
- 1992
- 1992
- English.
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In: Biochemical Journal. - 0264-6021 .- 1470-8728. ; 288:Pt 2, s. 625-629
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http://www.ncbi.nlm....
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Abstract
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- 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.
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