INFLUENCE OF BETA- ADRENERGIC RECEPTOR IN INSULIN RELEASE: A REVIEW

β-Adrenergic receptors (βARs) are a class of G-protein-coupled receptors (GPCRs) that bind to epinephrine and norepinephrine to mediate a physiological response. These receptors are divided into three subtypes: β1-AR, which is mainly found in the heart and brain; β2-AR, which is more widely distributed; and β3-AR, which is mainly found in adipose tissue. Generally, these receptors couple to Gαs to stimulate adenylyl cyclase; however, under certain conditions, they can couple to Gαi to inhibit adenylyl cyclase (AC) in some cells. β-Adrenergic receptors can both induce and ameliorate insulin resistance, depending on the receptor subtype, the duration of stimulation, and the type of tissue affected. Systemic use of β2-agonists can result in acute insulin resistance, while long-term use can improve it. These opposing effects may be attributed to a shift from Gαs-coupling in short-term use to Gαicoupling in long-term. In addition, Gαi-coupling may mediate the insulin sensitizing effects by activating β-arrestin signaling, particularly in the liver and adipose tissue.