Regulation of hepatic gluconeogenesis and glycogenolysis by catecholamines in rainbow trout during environmental hypoxia.

This study tests the hypothesis that catecholamines regulate glucose availability during hypoxia in the rainbow trout by activating glycogen phosphorylase (GPase) while inhibiting pyruvate kinase (PK) in the liver. The net result would be an increase in liver glycogenolysis and a reduction of glycolysis and/or enhancement of gluconeogenesis. We used the criteria of Stalmans & Hers (1975) and report much lower resting percent GPase a (active) values (20-30%) than those previously published. Dorsal aortic injections of epinephrine or norepinephrine increased plasma glucose (16-46%), had no effect on liver or muscle glycogen levels, decreased the activity of PK, and increased total and percent GPase a activities. Pre-treatment with the beta-adrenoreceptor antagonist propranolol eliminated these effects. During moderate hypoxia, plasma glucose remained unchanged, while lactate levels increased fourfold. When fish were pre-treated with propranolol, hypoxia depressed plasma glucose levels (-26%), total and percent GPase a, and increased PK activity, suggesting that hypoxia mediated the dephosphorylation of these enzymes. We conclude that catecholamines stimulate hepatic beta-adrenoreceptors during hypoxia and sustain plasma glucose levels by nullifying the deleterious effects of hypoxia on metabolic function. The specific metabolic consequences of these catecholamine-mediated effects are an increase in the activity of the active form of GPase and a reduction in PK activity, which suggests an activation of glycogenolysis and an inhibition of glycolysis and/or activation of gluconeogenesis, respectively.