Hormonal regulation of metabolism in hepatocytes of the ureogenic teleostopsanus beta.

Short-term exposure of isolated toadfish hepatocytes to high concentrations (100 nM) of glucagon, glucagon-like peptide (GLP) or epinephrine significantly increases the rate of lactate gluconeogenesis (1.3-fold) and glycogenolysis (5- to 7-fold). Half-maximal responsiveness to GLP is reached at about 2 nM for gluconeogenesis and 6 nM for glycogenolysis, while the value for glycogenolysis activated by catfish glucagon is 28 nM. Cells do not to respond to 5 nM epinephrine. Norepinephrine, urotensin II and leucine-enkephalin, each applied at 100 nM, increase the rate of glycogenolysis by 1.3 to 1.5-fold. All other hormones tested (vasotocin, isotocin, VIP, methionine-enkephalin, ovine prolactin, β-endorphin, APY, salmon insulin) failed to affect metabolic flux through glycogenolysis or gluconeogenesis. None of the hormones altered the rate of urea synthesis or the rate of lactate oxidation by hepatocytes. Although toadfish hepatocytes are responsive to hormonal stimuli, they do not appear to be a useful model to study evolutionary trends in short-term hormonal regulation of urea synthesis. However, the obvious differences in mechanisms of control of urea synthesis in this species compared with ureogenic amphibians and mammals open an intriguing avenue for research.