Glucose induces the discharge of insulin from the β-cell probably by acting on a specific cell membrane receptor. This then transmits the insulinogenic signal of glucose to the release mechanisms of the cell, probably via the adenyl cyclase-cyclic AMP system. Thus, in the β-cell, glucose acts not only as a substrate – as in every other type of cell – but also exerts a »hormone-like« action. In the present study, the relation of this hypothetic glucose receptor to the adrenergic receptor of the β-cell has been investigated. In 16 healthy subjects, blockade of the β-adrenergic receptors by iv infusion of propranolol resulted in significant inhibition of the initial as well as of late insulin responses to glucose infusion. This inhibition was partially reversed when aminophylline was administered together with propranolol. Blockade of the α-adrenergic receptors with phentolamine had no significant effect on the glucose induced insulin release. These findings suggest that the glucose receptor of the β-cell is closely related to the β-adrenergic receptor, propranolol being capable of interfering with the transmission of the insulinogenic signal of glucose. It cannot be excluded, however, that propranolol acts in an unspecific way, e. g., by stabilizing the cell membrane or by blocking adenyl cyclase, actions which by themselves may lead to the inhibition of insulin secretion.