A β-blockade, propranolol, was found to reduce lipogenesis from glucose stimulated by insulin in mice, suggesting that it inhibited an insulin action in vivo. When nicomol was administered with the blockade, its inhibitory action on insulin was remarkably relieved. It was demonstrated that propranolol also inhibited insulin-stimulated lipogenesis from glucose in isolated fat cells. In contrast to the in vivo experiments, nicomol did not relieve the inhibitory action on insulin in the fat cell system. On the other hand, nicotinic acid, one of metabolites of nicomol, was found to reduce the inhibitory action of propranolol on insulin. Then experiments were carried out to clarify the effect of micomol and its metabolites on PGI₂ and TXA₂ formation in the platelet rich plasma-arterial ring system. Nicomol was found to elevate PGI₂ level and reduce TXA₂ level in this system. On the other hand, nicotinic acid did not affect both PGI₂ and TXA₂ formation. Nicotinamide, one of metabolites of nicomol, increase PGI₂ formation, but did not affect TXA₂ content. Based on these experimental results, clinical effects of nicomol were discussed.