Beta adrenergic regulation of rat liver glycogenolysis during aging

Studies from a number of laboratories demonstrate a biphasic change in β adrenergic regulation of hepatic glycogenolysis over the life span of the male rat. The β adrenergic response is prominent in immature animals, declines rapidly during subsequent development to a minimum by the time of young adulthood, and then reemerges during postmaturational development. Age changes in β adrenergic-responsive adenylate cyclase activity follow a “U”-shaped curve similar to that described by changes in liver glycogenolytic responsiveness during aging. Developmental and postmaturational changes in β adrenergic-sensitive adenylate cyclase activation are related to parallel alterations in the density of β adrenergic receptors and also to functional changes in nonreceptor components of the enzyme. The prevailing view that catecholamines stimulate hepatic glycogenolysis by an α adrenergic receptor-mediated, cyclic AMP-independent mechanism is based almost entirely on evidence from young adult male rats. We propose that current concepts of α adrenergic-responsive liver glycogenolysis underestimate a physiological role for β adrenergic responsiveness over the majority of the life span.