Adrenergic receptors are not mediators in the lipolytic effect of somatostatin in rat adipocytes

Abstract Beta-adrenergic receptors have been purported to act as possible mediators in the lipolytic effect of somatostatin in vivo. Investigations with isolated rat adipocytes studying the lipolytic activity of somatostatin (1.7×10 −7 M), glucagon (8.1×10 −8 M) and norepinephrine (10 −6M ), have shown that the lipolytic effect stimulated by somatostatin is not altered by 10 −5 M propanolol (beta-antagonist); is significantly enhanced by 10 −5 M isoproterenol (beta-agonist) and is not altered by the addition of 10 −6 M phenoxybenzamine (alpha-antagonist) or 10 −6 M phenylephrine (alpha-agonist). Similar results were found when lipolysis was stimulated by glucagon, whereas the lipolytic effect stimulated by norepinephrine was blocked by propanolol. These results indicate that the direct lipolytic effect of somatostatin on isolated rat adipocytes does not seem to be mediated through mechanisms involved with adrenergic receptors.