α-Adrenoceptor-mediated glucose release from perifused catfish hepatocytes

Abstract

In fish liver catecholamines bind to β-adrenoceptors (AR) and increase glucose release via cAMP augmentation, α 1-AR have recently been shown to mediate IP 3 and Ca 2+ elevation in catfish and eel hepatocytes, although their coupling to a physiological response has remained doubtful. We have perifused isolated catfish hepatocytes in Bio-Gel P4 columns with epinephrine in the presence of prazosin and/or propranolol, α- and β-AR antagonists, respectively. Ten nM epinephrine stimulated glucose release approximately 3-fold, and this effect was completely antagonized by the simultaneous presence of both α- and β-AR blockers. The two AR antagonists separately inhibited about one-third and two-third of the total stimulation, respectively. Through α-AR occupancy, epinephrine provoked a significant increase of glucose release whereas no stimulation was detected in Ca 2+-depleted hepatocytes. Glucose release was strongly elevated by both ionomycin and dibutyryl cAMP. These results represent the first direct evidence that α-AR transduction pathway is involved in epinephrine-induced glucose release from fish hepatocytes.