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Desensitization of beta-adrenergic responses in adipocytes involves receptor subtypes and cAMP phosphodiesterase

, : Desensitization of beta-adrenergic responses in adipocytes involves receptor subtypes and cAMP phosphodiesterase. European Journal of Pharmacology 289(2): 235-247

Acute exposure of isolated adipocytes to isoproterenol induces the desensitization of lipolytic responses to norepinephrine and selective beta-1-, beta-2-- and beta-3-adrenoceptor agonists, as well as the adrenocorticotropic hormone 1-24 fragment (ACTH). Forskolin and 8-bromo-cAMP responses are also desensitized. When lipolysis was measured in the presence of OPC 3911 (N-cyclohexyl-N-2-hydroxyethyl-4(6-(1,2-dihydro-2-oxoquinolyloxy))butyramide), a specific inhibitor of the cAMP phosphodiesterase of adipocytes, the desensitization of all lipolytic agents -- except the beta-2-adrenoceptor agonist - was abolished. Isoproterenol induced a similar loss (35%) of both membrane beta-1- and beta-2-adrenoceptors and an uncoupling of beta-1-adrenoceptors, but did not modify the weak coupling of control beta-2-adrenoceptors. These data suggest that isoproterenol induced (i) an activation of the cAMP phosphodiesterase, which is solely responsible for the desensitization of norepinephrine response as well as beta-1- and beta-3-adrenoceptor mediated responses and (ii) an additional desensitization of the sole beta-2-adrenergic signaling system which suggests a subtype-selective pattern of regulating processes.


PMID: 7621897

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