In fish liver catecholamines bind to β-adrenoceptors (AR) and increase glucose release via cAMP augmentation, α1 -AR have recently been shown to mediate IP3 and Ca2+ 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 Ca2+-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.
alpha-adrenoceptor-mediated glucose release from perifused catfish hepatocytes
BIONDI, Carla;CAPUZZO, Antonio
1999
Abstract
In fish liver catecholamines bind to β-adrenoceptors (AR) and increase glucose release via cAMP augmentation, α1 -AR have recently been shown to mediate IP3 and Ca2+ 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 Ca2+-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.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.