SUPPRESSION OF VLDL-TRIACYLGLYCEROL SECRETION B Y BOTH α AND β-ADRENOCEPTOR AGONISTS IN ISOLATED RAT HEPATOCYTES

The effects of alpha and beta-adrenergic stimulation on triacylglycerol secretion were investigated in isolated rat hepatocytes. Epinephrine within 3h of incubation suppressed triacylglycerol secretion by 35% and increased its cellular content by 18%. The inhibitory effect of epinephrine was abolished by inclusion of phentolamine and also prazosin but not with propranolol. Trifluoperazine concealed the inhibitory effect of epinephrine in a dose-dependent manner, whereas theobromine did not have any significant effect. The secretion of triacylglycerol was suppressed not only by the a-agonist phenylephrine but also by the β-agonist isoproterenol. Dibutyryl-cyclic AMP also inhibited secretion of triacylglycerol by approximately 30%. The results indicate that epinephrine suppressed triacylglycerol secretion via the α1-adrenoceptor whereas stimulation of beta-as well as alpha-adrenoceptors can exert a similar effect. Calcium-calmodulin dependent protein kinase may be involved in the down-regulation of VLDL secretion. The unexpected effect of isoproterenol has been discussed in relation to "dual signaling" and also the "store-dependent calcium entry" hypotheses.