Metabolic effects of carvedilol through beta-arrestin proteins: investigations in a streptozotocin-induced diabetes rat model and in C2C12 myoblasts

Background and Purpose Carvedilol is a third-generation beta-adrenoceptor antagonist, which also stimulates beta-arrestins. beta-arrestins initiate intracellular signalling and are involved in insulin release and sensitivity. Carvedilol is superior in effectiveness to other drugs that are used for similar indications and does not cause insulin resistance or diabetes, which can occur with other beta-antagonists. We have shown that carvedilol increased glucose usage in C2C12 cells. We investigate the biased agonist efficacy of carvedilol on beta-arrestins.