Lack of correlation between catecholamine effects on cyclic adenosine 3':5'-monophosphate and gluconeogenesis in isolated rat liver cells.

Isolated liver cells from fasted female rats synthesized glucose in the presence of alanine, lactate, and pyruvate. Epinephrine, norepinephrine, and phenylephrine stimulated gluconeogenesis whereas isoproterenol and salbutamol had no effect on gluconeogenesis from lactate. Dand L-Propranolol had no effect on epinephrine-stimulated gluconeogenesis but blocked cyclic adenosine 3’:5’-monophosphate (cyclic AMP) accumulation due to epinephrine. Phentolamine had little effect on epinephrinestimulated cyclic AMP accumulation of gluconeogenesis by liver cells. Phenoxybenzamine also had no effect on epinephrine-stimulated cyclic AMP accumulation but did slightly reduce gluconeogenesis due to epinephrine. Low concentrations of dihydroergotamine decreased epinephrineand norepinephrine-stimulated gluconeogenesis but did not alter that due to dibutyryl cyclic AMP or glucagon. Dihydroergotamine did not reduce the increase in cyclic AMP accumulation due to epinephrine. Isoproterenol alone increased cyclic AMP but did not stimulate gluconeogenesis nor block the effect of epinephrine. Cycloheximide and dactinomycin did not inhibit epinephrine-stimulated gluconeogenesis by the cells. The fairly rapid onset of epinephrine stimulation of gluconeogenesis and the results with inhibitors suggest that RNA and protein synthesis are not required for the epinephrine action. The data also indicate that the increase in cyclic AMP accumulation due to epinephrine is apparently unrelated to its stimulation of gluconeogenesis in rat liver cells.