Potentiation of beta-adrenoceptor agonist-mediated lipolysis by quercetin and fisetin in isolated rat adipocytes.
Quercetin and fisetin, two naturally occurring bioflavonoids mobilized lipids and enzymes in the absence or presence of epinephrine in intact rat adipocytes. Dose-(0-250 microM) and time-(0-2 hr) course studies, showed that they stimulated phosphodiesterase (PDE) activity and simultaneously exert cyclic AMP accumulation. These bioflavonoids when present either singly or together with epinephrine stimulated the membrane-bound PDE but not the cytosolic PDE. The stimulation may act as a feedback mechanism to terminate the cyclic AMP effects. The action of theophylline, a known lipolytic agent (exerting its effects through antagonism of adenosine A1 receptor as well as PDE inhibition) was not potentiated by either fisetin or quercetin. However, the flavonoids potentiated epinephrine or isoproterenol- (a specific beta-adrenoreceptor agonist) induced lipolysis. Their effects were inhibited by propranolol (a beta-receptor antagonist). These results suggest that the flavonoids act synergistically with epinephrine on beta-adrenergic receptor and not through phosphodiesterase inhibition to stimulate adipocyte lipolysis. Increase in membrane phospholipid methylation occurred as a consequence of the epinephrine and/or quercetin/fisetin actions, and it correlated with the cellular accumulation of cyclic AMP.[1]References
- Potentiation of beta-adrenoceptor agonist-mediated lipolysis by quercetin and fisetin in isolated rat adipocytes. Kuppusamy, U.R., Das, N.P. Biochem. Pharmacol. (1994) [Pubmed]
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