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Insulin‐mediated sensitization of adenylyl cyclase activation
Author(s) -
Feldman Ross D.
Publication year - 1993
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1993.tb14013.x
Subject(s) - adenylyl cyclase , forskolin , medicine , endocrinology , adcy9 , insulin , adcy10 , camp dependent pathway , gs alpha subunit , cyclase , insulin receptor , receptor , chemistry , biology , insulin resistance
1 Insulin may be an important regulator of vascular function. We have previously studied lymphocyte β‐adrenoceptors as a model for the human vascular β‐adrenoceptor. To examine the effects of insulin on human β‐adrenoceptor responsiveness, adenylyl cyclase activity, cyclic AMP‐dependent protein kinase activity and β‐adrenoceptor radioligand binding assays were performed on permeabilized mononuclear leukocytes. 2 With acute exposure to insulin in vitro , followed by washing and permeabilization there was a dose‐dependent increase in both lymphocyte NaF‐stimulated activity and β‐adrenoceptor‐stimulated adenylyl cyclase activity paralleling an increase in β‐adrenoceptor‐stimulated protein kinase A activity. Manganese‐, forskolin‐ and forskolin plus guanylimidodiphosphate‐stimulated adenylyl cyclase activities were not altered by insulin pretreatment. Additionally, mononulcear leukocyte β‐adrenoceptor density, proportion of externalized receptors and receptor affinity for agonist were not altered. 3 The data indicate that acute exposure to insulin sensitizes G‐protein‐stimulated adenylyl cyclase activity. These findings suggest a potential role for insulin in the regulation of β‐adrenoceptor responsiveness in man.