Effect of catecholamines and methylprednisolone on carbohydrate metabolism of dogs.

TLDR: It was concluded that in vivo the lactate mobilization limits gluconeogenesis from this source, and methylprednisolone pretreatment greatly potentiated the effect of epinephrine.

Abstract: Rates of glucose and of lactate production, and of gluconeogenesis from lactate were measured in unanaesthetized dogs with indwelling arterial and venous catheters. 2-t-glucose, l (+)-lactate-14C, or the mixture of the two were used as tracers according to the primed, constant infusion technique. Norepinephrine infusion had virtually no effect on carbohydrate metabolism. In the normal dog, epinephrine caused increases in plasma glucose levels (about 50%) and in glucose production (35%); lactate turnover increased nearly fourfold, and gluconeogenesis from lactate increased proportionally, thereby almost tripling the lactate contribution to glucose production. There was a logarithmic correlation between plasma lactate level and lactate turnover and a straight line correlation between lactate turnover and the rate of formation of glucose from lactate. The increase of lactate turnover after lactate infusion alone, and combined with norepinephrine, and after methylprednisolone treatment fitted the straight line correlation. It was therefore concluded that in vivo the lactate mobilization limits gluconeogenesis from this source. methylprednisolone pretreatment greatly potentiated the effect of epinephrine. Plasma glucose was increased to 300–600 mg 100 ml . Glucose production rose to four to eight times normal, and gluconeogenesis from lactate rose to eight to ten times the normal values.