The effect of elevated plasma epinephrine concentrations (≈800 pg/ml) on ketone body kinetics was determined in postabsorptive normal subjects using primed-continuous infusions of 3-14C-acetoacetate. Infusion of epinephrine (60 ng/kg/min) resulted in a transient increase in total ketone body production to a maximum of 2.5-fold the basal rate within 45 min (P < 0.01 versus controls). Ketone body uptake increased with a delay, compared with production, causing a 2.8-fold increase in total ketone body concentrations (P < 0.05 versus controls). Plasma free fatty acid (FFA) and blood glycerol concentrations increased transiently during epinephrine; their course was similar to that of ketone body production. Epinephrine administration resulted in hyperglycemie, hyperlactatemia, and a modest increase in plasma insulin and glucagon concentrations. To assess epinephrine's effect on ketone body kinetics during lack of insulin, and to avoid epinephrine-induced alterations in plasma insulin and glucagon concentrations, epinephrine was also infused combined with somatostatin (6.5 μg/kg/h). During somatostatin infusion, epinephrine administration resulted in an enhanced and sustained elevation of total ketone body production from 4.4 ± 0.8 to 15.1 ±1.2 μmol/kg/min (P < 0.01 versus somatostatin alone). Ketone body concentrations increased markedly from 310 ± 63 to 1763 ± 137 μmol/L (P < 0.01 versus somatostatin alone); the ketonemic effect was enhanced due to a 40% decrease of the metabolic clearance rate associated with somatostatin infusion. The increase in plasma FFA and blood glycerol concentrations during somatostatin-induced insulin deficiency was transiently enhanced by epinephrine, such that they increased to 3.2- and 5.6-fold their basal values after 45 min, respectively (P < 0.01). Thus, elevation of epinephrine concentrations to levels that are observed in severe stress resulted, in normal man, in a transient increase in lipolysis and ketogenesis. The metabolic clearance of ketone bodies increased initially but remained uninfluenced thereafter. The transient nature of the increase in ketogenesis and lipolysis was in part due to an elevation of plasma insulin levels caused by hyperglycemia. During acute insulin deficiency, epinephrine's effect on ketogenesis was sustained, while the acceleration of lipolysis was again transient, suggesting a direct hepatic ketogenic effect. However, the major influence of epinephrine on ketone body kinetics consisted of an enhancement of ketone body production secondary to an increase in lipolysis and FFA supply for ketogenesis.

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