Nutritional state modulates hormone‐mediated hepatic glycogenolysis in chinook salmon (Oncorhynchus tshawytscha)

Juvenile chinook salmon were used to investigate the interaction of nutritional state and hormones (glucagon, epinephrine) on hepatic glycogenolysis. Experiments were conducted in vitro on liver removed from animals of varying nutritional states: fed 1 week, fasted 1 week, fed 3 weeks, fasted 3 weeks, and fasted 1 week/refed 2 weeks. Basal glycogen breakdown in liver isolated from continuously fed (1 week and 3 weeks) fish proceeded at insignificant levels, whereas glycogen breakdown in liver isolated from fasted animals progressed rapidly during the course of incubation. However, no difference in the pattern of glycogen breakdown between liver isolated from animals fasted for 1 week and those fasted for 3 weeks was observed. The presence of glucose in the incubation medium retarded glycogen breakdown in the livers from fasted fish. Both epinephrine and glucagon stimulated glucose release from liver isolated from fish fed continuously and from fish fasted 1 week; epinephrine appeared more potent in this regard than glucagon. Epinephrine also stimulated glucose release from liver isolated from fish fasted 3 weeks, whereas glucagon was without significant glycogenolytic effect on this tissue. Insulin inhibited epinephrine‐ and glucagon‐stimuluated glucose release. These results suggest that glucagon plays a role in modulating nutrition‐associated adjustments in metabolism during the early stages of fasting and that, with extended fasting, the liver loses its sensitivity to glucagon with regard to glycogenolysis.